From v.evans from bangor.ac.uk Tue Jan 6 09:12:21 2009 From: v.evans from bangor.ac.uk (Vyv Evans) Date: Tue Jan 6 13:26:36 2009 Subject: [Neuroscience] Receive LANGUAGE & COGNITION free of charge Message-ID: <496366C5.6070207@bangor.ac.uk> NEW JOURNAL --- LANGUAGE & COGNITION --- SPECIAL OFFER FOR 2009 The first volume of the new journal LANGUAGE AND COGNITION appears this year. As a special offer the entire first volume (two issues) is offered as a downloadable e-file free of charge, and is available to all. To take advantage register to receive your free copy now! Full details of how to register can be found on the journal website: www.languageandcognition.net Table of contents for volumes 1 and 2, is available below. LANGUAGE AND COGNITION is a venue for the publication of high quality peer-reviewed research of a theoretical and/or empirical/experimental nature, focussing on the interface between language and cognition. The journal publishes research from the full range of subject disciplines, theoretical backgrounds, and analytical frameworks that populate the language and cognitive sciences, on a wide range of topics. Research published in the journal typically adopted an interdisciplinary, comparative, multi-methodological approach to the study of language and cognition and their intersection. The journal is edited by Daniel Casasanto, Seana Coulson, Vyvyan Evans, David Kemmerer, Laura Michaelis and Chris Sinha. The journal is open to contributions from any theoretical perspective and methodological approach which bears on the scientific study of language and its relationship with cognition. In particular it publishes both theoretical and empirical research. Submission details can be found on the journal website: www.languageandcognition.net TABLE OF CONTENTS VOLUME 1 (2009) Issue 1 How do infants build a semantic system? Suzy J. Styles and Kim Plunkett (University of Oxford) The cognitive poetics of literary resonance. Peter Stockwell (University of Nottingham) Action in cognition: The case of language. Lawrence J. Taylor and Rolf A. Zwaan (Erasmus University of Rotterdam) Prototype constructions in early language acquisition. Paul Ibbotson (University of Manchester) and Michael Tomasello (MPI for Evolutionary Anthropology, Leipzig) The Enactment of Language: Decades of Interactions Between Linguistic and Motor Processes. Sarah E. Anderson (Cornell University) and Michael J. Spivey (University of California, Merced) Episodic affordances contribute to language comprehension. Arthur M. Glenberg (Arizona State Universtiy), Raymond Becker (Wilfrid Laurier University), Susann Klötzer, Lidia Kolanko, Silvana Müller (Dresden University of Technology), and Mike Rinck (Radboud University Nijmegen) Reviews: Daniel D. Hutto. 2008. Folk Psychological Narratives: The Sociocultural Basis of Understanding Reasons (MIT Press). Reviewed by Chris Sinha Aniruddh Patel. 2008. Music, Language, and the Brain (Oxford Univeristy Press). Reviewed by Daniel Casasanto Issue 2 Pronunciation reflects syntactic probabilities: Evidence from spontaneous speech. Hal Tily (Stanford University), Susanne Gahl (University of California, Berkeley), Inbal Arnon, Neal Snider, Anubha Kothari, and Joan Bresnan (Stanford University) Causer subjects in English, Korean and Chinese and the individuation of events. Phillip Wolff, Ga-hyun Jeon, and Yu Li (Emory University) Correlation versus prediction in children’s word learning: Cross-linguistic evidence and simulations. Eliana Colunga (University of Colorado at Boulder), Linda B. Smith (Indiana University) and Michael Gasser (Indiana University) Toward a theory of word meaning. Gabriella Vigliocco, Lotte Meteyard and Mark Andrews (University College London) The sensory-motor theory of semantics: A functional imaging perspective. Uta Noppeney (MPI for Biological Cybernetics, Tuebingen) Reviews: Ronald Langacker. 2008. Cognitive Grammar: A basic introduction. (Oxford University Press). Reviewed by Vyvyan Evans Giacomo Rizzolatti and Corrado Sinigagalia. Mirrors in the brain: How our minds share actions and emotions. 2008. (Oxford University Press). Reviewed by David Kemmerer. VOLUME 2 (2010) Issue 1 Adaptive cognition without massive modularity: The context-sensitivity of language use. Raymond W. Gibbs (University of California, Santa Cruz) and Guy Van Orden (University of Cincinnati) Spatial foundations of the conceptual system. Jean Mandler (University California, San Diego and University College London) Metaphor: Old words, new concepts, imagined worlds. Robyn Carston (University College London) Language Development and Linguistic Relativity. John A. Lucy (University of Chicago) Construction Learning. Adele Goldberg (Princeton University) Space and Language: some neural considerations. Anjan Chatterjee (University of Pennsylvania) Issue 2 Abstract motion is no longer abstract. Teenie Matlock (University California, Merced) When gesture does and doesn't promote learning. Susan Goldin-Meadow (University of Chicago) Discourse Space Theory. Paul Chilton (Lancaster University) Relational language supports relational cognition. Dedre Gentner (Northwestern University) Talking about quantities in space. Kenny Coventry (Northumbria University) Making sense of language: Insights from cognitive science research. Jos van Berkum (MPI for Psycholinguistics, Nijmegen) Précis of The Genesis of Grammar. Bernd Heine (University of Cologne) and Tania Kuteva (Heinrich Heine University) -- Gall y neges e-bost hon, ac unrhyw atodiadau a anfonwyd gyda hi, gynnwys deunydd cyfrinachol ac wedi eu bwriadu i'w defnyddio'n unig gan y sawl y cawsant eu cyfeirio ato (atynt). Os ydych wedi derbyn y neges e-bost hon trwy gamgymeriad, rhowch wybod i'r anfonwr ar unwaith a dilëwch y neges. Os na fwriadwyd anfon y neges atoch chi, rhaid i chi beidio â defnyddio, cadw neu ddatgelu unrhyw wybodaeth a gynhwysir ynddi. Mae unrhyw farn neu safbwynt yn eiddo i'r sawl a'i hanfonodd yn unig ac nid yw o anghenraid yn cynrychioli barn Prifysgol Bangor. Nid yw Prifysgol Bangor yn gwarantu bod y neges e-bost hon neu unrhyw atodiadau yn rhydd rhag firysau neu 100% yn ddiogel. Oni bai fod hyn wedi ei ddatgan yn uniongyrchol yn nhestun yr e-bost, nid bwriad y neges e-bost hon yw ffurfio contract rhwymol - mae rhestr o lofnodwyr awdurdodedig ar gael o Swyddfa Cyllid Prifysgol Bangor. www.bangor.ac.uk This email and any attachments may contain confidential material and is solely for the use of the intended recipient(s). If you have received this email in error, please notify the sender immediately and delete this email. If you are not the intended recipient(s), you must not use, retain or disclose any information contained in this email. Any views or opinions are solely those of the sender and do not necessarily represent those of the Bangor University. Bangor University does not guarantee that this email or any attachments are free from viruses or 100% secure. Unless expressly stated in the body of the text of the email, this email is not intended to form a binding contract - a list of authorised signatories is available from the Bangor University Finance Office. www.bangor.ac.uk From johnh from goawayplease.com Thu Jan 8 09:44:40 2009 From: johnh from goawayplease.com (John Hasenkam) Date: Thu Jan 8 12:24:01 2009 Subject: [Neuroscience] Re: SSRIs bind to post-synaptic 5-HT receptors and function as competitive antagonists? References: <49234c1f$0$26361$ed362ca5@nr5.newsreader.com> <4923e9c8$0$26332$ed362ca5@nr5.newsreader.com> <1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com> <4924ad7c$0$28062$ed362ca5@nr5.newsreader.com> Message-ID: <-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au> Hey Glen, Would you mind posting your provisional answer? Depression is a hobby horse of mine and given recent controversy over just how SSRIs do what they do I'm interested. Trust the musical marvel is doing well. John. > I can now answer my own question, but I'll post the provisional answer for > those that might be interested, and I'll provide a reference for those > that are interested. Some SSRIs do, indeed, bind at the 5-HT2c receptor, > and function as competitive antagonists. "Glen M. Sizemore" wrote in message news:4924ad7c$0$28062$ed362ca5@nr5.newsreader.com... > > "r norman" wrote in message > news:1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com... >> On Wed, 19 Nov 2008 05:26:55 -0500, "Glen M. Sizemore" >> wrote: >> >>> >>>"Glen M. Sizemore" wrote in message >>>news:49234c1f$0$26361$ed362ca5@nr5.newsreader.com... >>>> Someone I know claims that SSRIs bind at post-synaptic serotonin >>>> receptors, and function as competitive antagonists. Anyone know >>>> anything >>>> about this? Thanks ahead of time... >>>> >>>> G. >>> >>>Correction: SOME SSRIs >> >> Could (s)he be thinking of the action of pindolol which is sometimes >> used in conjunction with SSRIs? > > Hi Dr. Norman, > > I can now answer my own question, but I'll post the provisional answer for > those that might be interested, and I'll provide a reference for those > that are interested. Some SSRIs do, indeed, bind at the 5-HT2c receptor, > and function as competitive antagonists. > > Cordially, > Glen From gmsizemore2 from yahoo.com Fri Jan 9 05:21:04 2009 From: gmsizemore2 from yahoo.com (Glen M. Sizemore) Date: Fri Jan 9 12:36:53 2009 Subject: [Neuroscience] Re: SSRIs bind to post-synaptic 5-HT receptors and function as competitive antagonists? In-Reply-To: <-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au> References: <49234c1f$0$26361$ed362ca5@nr5.newsreader.com> <4923e9c8$0$26332$ed362ca5@nr5.newsreader.com> <1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com> <4924ad7c$0$28062$ed362ca5@nr5.newsreader.com> <-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au> Message-ID: <49672529$0$24851$ed362ca5@nr5c.newsreader.com> "John Hasenkam" wrote in message news:-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au... > Hey Glen, > > Would you mind posting your provisional answer? Depression is a hobby > horse of mine and given recent controversy over just how SSRIs do what > they do I'm interested. > > Trust the musical marvel is doing well. > > > John. Hi John, I am trying to get to the bottom of this alleged binding of some SSRIs to the 5-HT2c receptor - I may have spoken too soon! I'll get back to you on this. I am going to have to become educated on this topic since I am going to be involved in the pre-clinical anti-depressant business. What are you referring to when you talk about the "recent controversy"? Yes, Mike is doing well - he's become sort of good on the sax (just a hobby though). He went to see Perlman the other night - he was supposed to get to meet him before the performance, but Perlman was not up to meeting people. Mike spends a lot of time watching Perlman and old tapes of Heifetz - that's in between times when he is teaching himself to play drums along with an old Little Feat LP we have. Hope you are well. Regards, Glen > > >> I can now answer my own question, but I'll post the provisional answer >> for those that might be interested, and I'll provide a reference for >> those that are interested. Some SSRIs do, indeed, bind at the 5-HT2c >> receptor, and function as competitive antagonists. > > > > "Glen M. Sizemore" wrote in message > news:4924ad7c$0$28062$ed362ca5@nr5.newsreader.com... >> >> "r norman" wrote in message >> news:1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com... >>> On Wed, 19 Nov 2008 05:26:55 -0500, "Glen M. Sizemore" >>> wrote: >>> >>>> >>>>"Glen M. Sizemore" wrote in message >>>>news:49234c1f$0$26361$ed362ca5@nr5.newsreader.com... >>>>> Someone I know claims that SSRIs bind at post-synaptic serotonin >>>>> receptors, and function as competitive antagonists. Anyone know >>>>> anything >>>>> about this? Thanks ahead of time... >>>>> >>>>> G. >>>> >>>>Correction: SOME SSRIs >>> >>> Could (s)he be thinking of the action of pindolol which is sometimes >>> used in conjunction with SSRIs? >> >> Hi Dr. Norman, >> >> I can now answer my own question, but I'll post the provisional answer >> for those that might be interested, and I'll provide a reference for >> those that are interested. Some SSRIs do, indeed, bind at the 5-HT2c >> receptor, and function as competitive antagonists. >> >> Cordially, >> Glen > > From johnh from goawayplease.com Fri Jan 9 08:22:53 2009 From: johnh from goawayplease.com (John Hasenkam) Date: Fri Jan 9 12:37:07 2009 Subject: [Neuroscience] Re: SSRIs bind to post-synaptic 5-HT receptors and function as competitive antagonists? References: <49234c1f$0$26361$ed362ca5@nr5.newsreader.com> <4923e9c8$0$26332$ed362ca5@nr5.newsreader.com> <1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com> <4924ad7c$0$28062$ed362ca5@nr5.newsreader.com> <-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au> <49672529$0$24851$ed362ca5@nr5c.newsreader.com> Message-ID: <0_ednaYTzJUf0vrUnZ2dnUVZ8srinZ2d@westnet.com.au> 1. Recent controversy: I've just finished reading Prozac Backlash(2000) by Glenmullen, a Harvard based psychiatrist who claims SSRIs carry all sorts of risks. There are some risks involved but generally quite slight, though the issue of Redux is worrying. It was an SSRI for appetite suppression but was found to destroy serotonergic axons. Interesting given the known neurotoxicity of Ecstasy and that it is a strong serotonin agonist. In addition recent studies on mice found that mice raised on prozac grow up displaying depressive like symptoms. I think Glenmullen is way over the top but still have serious concerns about the widespread use of SSRIs in children. I am not against antidepressants, in fact I consider these drugs to be a great benefit, but I have concerns about the excessive reliance on these drugs. Effexor can induce serious withdrawal symptoms, I don't care what the authorities say I've heard enough people describe their SSRI as a "security blanket" to wonder if this is not a manifestation of dependency. In fact the general advice now is that one should never abruptly stop taking these drugs because of potential withdrawal problems. Whoops, that should read ... because of a potential "antidepressant discontinuation syndrome". Ha! What is now being discovered is that CBT\psychotherapy is not only just as effective in treating depression but appears to be much better at preventing relapses. In fact SSRI's can only prevent relapses if one stays on the drugs, which might explain why so many patients are on these for life. Additionally, even strategies like insight meditation, exercise, and dietary changes can be very helpful in dealing with depression. Even vitamin D status may be of slight value because it inhibits pro-inflammatory cytokine production. Then there is the Lancet study which found slight increases in serotonin levels from sunshine exposure, this probably relating to the changes in the melatonin - serotonin balance. Mt is produced from serotonin, Mt production is rapidly stopped by sunlight exposure(amacrine cells in retina, circadians, all that jazz), and Mt can induce drowsiness and fatigue. That brings us to circadians, loss of circadian stability is an intrinsic stressor, you can see the increase in pro-inflammatory cytokines and for some depressives the loss of circadian stability and hence sleep patterns is the straw that makes one rush for a pill. Not surprising, even short periods of sleep deprivation can significantly enhance the production of pro-inflammatory cytokines and this has serious implications not just for depression but for cancer, dementia, cardiovascular disease and what else??? The most remarkable result I have read on the circadian issue was in relation to airline staff who crossed timelines and experienced persistent circadian disruption but without sleep deprivation. 5 year study found differences in temporal lobe volumes and cognitive scores. 2. I'm also wondering if the "competitive antagonist" = inverse agonist. These ligands bind the receptor, change its conformation, and thereby prevent second messenger\adaptor proteins coming into play when a agonist ligand attaches to the receptor. I haven't had time to look into this but the 5HT2c receptor appears to activate production of arachidonic acid(need to find quantifiers for the degree of production), a known pro-inflammatory mediator because it paves the way for pge 2, which in turns helps maintain the expression of pro-inflammatory cytokines(eg. il1, tnfa, il6 is tricky, can work both ways). What is not that well known is that depression can involve substantial increases in pro-inflammatory cytokines and it appears that trying to understand depression by sole reference to the CNS is doomed to fail. Keynote article: Cytokines and Depression: the need for a new paradigm. I have this buried in my archives. We must consider endocrine and immunological impacts as well. In regard to this Sapolsky et al has a great review article, I need to read that again ... . The reason omega 3 intake can help in depression, and possibly some other neuro disorders, is that EPA inhibits A. acid production, diverting the pathways to anti-inflammatory prostaglandins. What I have not looked into is how serotonin impacts on immunological function, many immune cells have 5HT receptors. For a very different perspective on these matters look up the ideas of David Horrobin, I have a seminal article of his in my archives, that would be a good starting point. If you so wish, give me some time, I'll email you some of these articles. PS: haven't looked too closely at depression for many years now so I'm rusty. I have a small mountain of data in my archives though so if you any specific queries email me and I'll see what I can do to help. Be well, John. "How many economists does it take to change a lightbulb? None, the invisible hand will do it." Citation: Mean markets and Lizard Brains. "Glen M. Sizemore" wrote in message news:49672529$0$24851$ed362ca5@nr5c.newsreader.com... > > "John Hasenkam" wrote in message > news:-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au... >> Hey Glen, >> >> Would you mind posting your provisional answer? Depression is a hobby >> horse of mine and given recent controversy over just how SSRIs do what >> they do I'm interested. >> >> Trust the musical marvel is doing well. >> >> >> John. > > Hi John, > I am trying to get to the bottom of this alleged binding of some SSRIs to > the 5-HT2c receptor - I may have spoken too soon! I'll get back to you on > this. I am going to have to become educated on this topic since I am going > to be involved in the pre-clinical anti-depressant business. What are you > referring to when you talk about the "recent controversy"? > > Yes, Mike is doing well - he's become sort of good on the sax (just a > hobby though). He went to see Perlman the other night - he was supposed to > get to meet him before the performance, but Perlman was not up to meeting > people. Mike spends a lot of time watching Perlman and old tapes of > Heifetz - that's in between times when he is teaching himself to play > drums along with an old Little Feat LP we have. > > Hope you are well. > > Regards, > Glen > > >> >> >>> I can now answer my own question, but I'll post the provisional answer >>> for those that might be interested, and I'll provide a reference for >>> those that are interested. Some SSRIs do, indeed, bind at the 5-HT2c >>> receptor, and function as competitive antagonists. >> >> >> >> "Glen M. Sizemore" wrote in message >> news:4924ad7c$0$28062$ed362ca5@nr5.newsreader.com... >>> >>> "r norman" wrote in message >>> news:1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com... >>>> On Wed, 19 Nov 2008 05:26:55 -0500, "Glen M. Sizemore" >>>> wrote: >>>> >>>>> >>>>>"Glen M. Sizemore" wrote in message >>>>>news:49234c1f$0$26361$ed362ca5@nr5.newsreader.com... >>>>>> Someone I know claims that SSRIs bind at post-synaptic serotonin >>>>>> receptors, and function as competitive antagonists. Anyone know >>>>>> anything >>>>>> about this? Thanks ahead of time... >>>>>> >>>>>> G. >>>>> >>>>>Correction: SOME SSRIs >>>> >>>> Could (s)he be thinking of the action of pindolol which is sometimes >>>> used in conjunction with SSRIs? >>> >>> Hi Dr. Norman, >>> >>> I can now answer my own question, but I'll post the provisional answer >>> for those that might be interested, and I'll provide a reference for >>> those that are interested. Some SSRIs do, indeed, bind at the 5-HT2c >>> receptor, and function as competitive antagonists. >>> >>> Cordially, >>> Glen >> >> > From kldickson from wisc.edu Fri Jan 9 13:55:30 2009 From: kldickson from wisc.edu (KATHARINE LEAH DICKSON) Date: Fri Jan 9 15:02:56 2009 Subject: [Neuroscience] Re: SSRIs bind to post-synaptic 5-HT receptors and function as competitive antagonists? In-Reply-To: <0_ednaYTzJUf0vrUnZ2dnUVZ8srinZ2d@westnet.com.au> References: <49234c1f$0$26361$ed362ca5@nr5.newsreader.com> <4923e9c8$0$26332$ed362ca5@nr5.newsreader.com> <1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com> <4924ad7c$0$28062$ed362ca5@nr5.newsreader.com> <-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au> <49672529$0$24851$ed362ca5@nr5c.newsreader.com> <0_ednaYTzJUf0vrUnZ2dnUVZ8srinZ2d@westnet.com.au> Message-ID: I'm curious as to why SSRIs are most effective in the severely depressed - at what point do antidepressants become more effective than talk therapy, if indeed for all but the most extreme depressions CBT is more effective, which seems to be the case? Is there a point where the neurochemical milieu in the brain necessitates antidepressant intervening? Katharine Leah Dickson kldickson@wisc.edu ----- Original Message ----- From: John Hasenkam Date: Friday, January 9, 2009 11:45 am Subject: [Neuroscience] Re: SSRIs bind to post-synaptic 5-HT receptors and function as competitive antagonists? To: neur-sci@magpie.bio.indiana.edu > 1. Recent controversy: > > I've just finished reading Prozac Backlash(2000) by Glenmullen, a > Harvard > based psychiatrist who claims SSRIs carry all sorts of risks. There > are some > risks involved but generally quite slight, though the issue of Redux > is > worrying. It was an SSRI for appetite suppression but was found to > destroy > serotonergic axons. Interesting given the known neurotoxicity of > Ecstasy and > that it is a strong serotonin agonist. In addition recent studies on > mice > found that mice raised on prozac grow up displaying depressive like > symptoms. I think Glenmullen is way over the top but still have > serious > concerns about the widespread use of SSRIs in children. I am not > against > antidepressants, in fact I consider these drugs to be a great > benefit, but I > have concerns about the excessive reliance on these drugs. Effexor > can > induce serious withdrawal symptoms, I don't care what the authorities > say > I've heard enough people describe their SSRI as a "security blanket" > to > wonder if this is not a manifestation of dependency. In fact the > general > advice now is that one should never abruptly stop taking these drugs > because > of potential withdrawal problems. Whoops, that should read ... > because of a > potential "antidepressant discontinuation syndrome". Ha! > > > What is now being discovered is that CBT\psychotherapy is not only > just as > effective in treating depression but appears to be much better at > preventing > relapses. In fact SSRI's can only prevent relapses if one stays on > the > drugs, which might explain why so many patients are on these for > life. > Additionally, even strategies like insight meditation, exercise, and > dietary > changes can be very helpful in dealing with depression. Even vitamin > D > status may be of slight value because it inhibits pro-inflammatory > cytokine > production. Then there is the Lancet study which found slight > increases in > serotonin levels from sunshine exposure, this probably relating to > the > changes in the melatonin - serotonin balance. Mt is produced from > serotonin, > Mt production is rapidly stopped by sunlight exposure(amacrine cells > in > retina, circadians, all that jazz), and Mt can induce drowsiness and > > fatigue. That brings us to circadians, loss of circadian stability is > an > intrinsic stressor, you can see the increase in pro-inflammatory > cytokines > and for some depressives the loss of circadian stability and hence > sleep > patterns is the straw that makes one rush for a pill. Not surprising, > even > short periods of sleep deprivation can significantly enhance the > production > of pro-inflammatory cytokines and this has serious implications not > just for > depression but for cancer, dementia, cardiovascular disease and what > else??? > The most remarkable result I have read on the circadian issue was in > > relation to airline staff who crossed timelines and experienced > persistent > circadian disruption but without sleep deprivation. 5 year study > found > differences in temporal lobe volumes and cognitive scores. > > 2. > > I'm also wondering if the "competitive antagonist" = inverse agonist. > These > ligands bind the receptor, change its conformation, and thereby > prevent > second messenger\adaptor proteins coming into play when a agonist > ligand > attaches to the receptor. I haven't had time to look into this but > the 5HT2c > receptor appears to activate production of arachidonic acid(need to > find > quantifiers for the degree of production), a known pro-inflammatory > mediator > because it paves the way for pge 2, which in turns helps maintain the > > expression of pro-inflammatory cytokines(eg. il1, tnfa, il6 is > tricky, can > work both ways). What is not that well known is that depression can > involve > substantial increases in pro-inflammatory cytokines and it appears > that > trying to understand depression by sole reference to the CNS is > doomed to > fail. Keynote article: Cytokines and Depression: the need for a new > paradigm. I have this buried in my archives. We must consider > endocrine and > immunological impacts as well. In regard to this Sapolsky et al has a > great > review article, I need to read that again ... . The reason omega 3 > intake > can help in depression, and possibly some other neuro disorders, is > that EPA > inhibits A. acid production, diverting the pathways to > anti-inflammatory > prostaglandins. What I have not looked into is how serotonin impacts > on > immunological function, many immune cells have 5HT receptors. > > For a very different perspective on these matters look up the ideas > of David > Horrobin, I have a seminal article of his in my archives, that would > be a > good starting point. If you so wish, give me some time, I'll email > you some > of these articles. > > PS: haven't looked too closely at depression for many years now so > I'm > rusty. I have a small mountain of data in my archives though so if > you any > specific queries email me and I'll see what I can do to help. > > Be well, > > John. > > "How many economists does it take to change a lightbulb? > None, the invisible hand will do it." > > Citation: Mean markets and Lizard Brains. > > > > > > "Glen M. Sizemore" wrote in message > news:49672529$0$24851$ed362ca5@nr5c.newsreader.com... > > > > "John Hasenkam" wrote in message > > news:-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au... > >> Hey Glen, > >> > >> Would you mind posting your provisional answer? Depression is a > hobby > >> horse of mine and given recent controversy over just how SSRIs do > what > >> they do I'm interested. > >> > >> Trust the musical marvel is doing well. > >> > >> > >> John. > > > > Hi John, > > I am trying to get to the bottom of this alleged binding of some > SSRIs to > > the 5-HT2c receptor - I may have spoken too soon! I'll get back to > you on > > this. I am going to have to become educated on this topic since I > am going > > to be involved in the pre-clinical anti-depressant business. What > are you > > referring to when you talk about the "recent controversy"? > > > > Yes, Mike is doing well - he's become sort of good on the sax (just > a > > hobby though). He went to see Perlman the other night - he was > supposed to > > get to meet him before the performance, but Perlman was not up to > meeting > > people. Mike spends a lot of time watching Perlman and old tapes of > > > Heifetz - that's in between times when he is teaching himself to > play > > drums along with an old Little Feat LP we have. > > > > Hope you are well. > > > > Regards, > > Glen > > > > > >> > >> > >>> I can now answer my own question, but I'll post the provisional > answer > >>> for those that might be interested, and I'll provide a reference > for > >>> those that are interested. Some SSRIs do, indeed, bind at the > 5-HT2c > >>> receptor, and function as competitive antagonists. > >> > >> > >> > >> "Glen M. Sizemore" wrote in message > >> news:4924ad7c$0$28062$ed362ca5@nr5.newsreader.com... > >>> > >>> "r norman" wrote in message > >>> news:1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com... > >>>> On Wed, 19 Nov 2008 05:26:55 -0500, "Glen M. Sizemore" > >>>> wrote: > >>>> > >>>>> > >>>>>"Glen M. Sizemore" wrote in message > >>>>>news:49234c1f$0$26361$ed362ca5@nr5.newsreader.com... > >>>>>> Someone I know claims that SSRIs bind at post-synaptic serotonin > >>>>>> receptors, and function as competitive antagonists. Anyone > know > >>>>>> anything > >>>>>> about this? Thanks ahead of time... > >>>>>> > >>>>>> G. > >>>>> > >>>>>Correction: SOME SSRIs > >>>> > >>>> Could (s)he be thinking of the action of pindolol which is sometimes > >>>> used in conjunction with SSRIs? > >>> > >>> Hi Dr. Norman, > >>> > >>> I can now answer my own question, but I'll post the provisional > answer > >>> for those that might be interested, and I'll provide a reference > for > >>> those that are interested. Some SSRIs do, indeed, bind at the > 5-HT2c > >>> receptor, and function as competitive antagonists. > >>> > >>> Cordially, > >>> Glen > >> > >> > > > > > _______________________________________________ > Neur-sci mailing list > Neur-sci@net.bio.net > http://www.bio.net/biomail/listinfo/neur-sci > From risto from cs.utexas.edu Fri Jan 9 17:26:11 2009 From: risto from cs.utexas.edu (Risto Miikkulainen) Date: Fri Jan 9 22:52:38 2009 Subject: [Neuroscience] WSOM-09 cognitive neuroscience session; Deadline extended to Feb 1 Message-ID: <200901092226.n09MQBZU020618@moro.cs.utexas.edu> The WSOM-2009 conference will feature a small number of special sessions. Of particular interest is the one on cognitive neuroscience: The special session on cognitive neuroscience focuses on computational models of self-organizing maps in the brain as well as cognitive processes based on such maps. The goal of such models is to gain insight into the development and function of the visual, somatosensory, and auditory cortex, as well as higher cognitive functions such as pattern recognition, memory, and language processing. Papers in this session may e.g. extend self-organizing maps with biological mechanisms such as spiking neurons, lateral connections, hierarchies, and feedback, or explain various biological or cognitive phenomena in terms of learning and processing on such maps. The deadline of WSOM 2009 has been extended to February 1st. -- Risto ---------------------------------------------------------------------- WSOM 2009 7th International Workshop on Self-Organizing Maps June 8-10, 2009 http://www.cnel.ufl.edu/conferences/WSOM2009/ Casa Monica Hotel, St. Augustine, Florida, USA http://www.casamonica.com Organizing Committee: General Chair: Jose Principe [principe@cnel.ufl.edu] Program Chair: Risto Miikkulainen [risto@cs.utexas.edu] OBJECTIVES WSOM'09 will be bringing together researchers and practitioners in the field of self-organizing systems, with a particular emphasis on neural networks and self-organizing maps. It will highlight key advances in these and related fields. It is the seventh conference in a series of bi-annual international conferences started with WSOM'97 in Helsinki. CALL FOR PAPERS The workshop will feature keynote addresses and technical presentations with recent advances in the area which will be collected in a CD-ROM distributed at the conference and that will be included in the registration. Papers are solicited for, but not limited to, the following areas: * Bioinformatics * Cognitive Modeling * Data visualization, mining and sonification * Financial analysis * Hardware and architecture * Neuroscience * Optimization * Robotics and Intelligent Systems * Self-organization * Signal processing, image processing and vision * Text and document analysis * Theory and extensions * Time-series analysis * Unsupervised learning (including PCA/NLPCA, ICA/NLICA, Principal Curves/Surfaces) SCHEDULE Submission of full papers: February 1, 2009 (deadline extended) Notification of acceptance: March 1, 2009 Camera-ready papers, author registration: April 2, 2009 Advance registration deadline: April 15, 2009 PAPER FORMAT Submissions may be up to nine pages in length, including figures and references, in single-column format, using a font no smaller than 10 points, except for the abstract, a font of 9 points may be used. Please refer to the conference website for further details. REVIEW PROCEDURE All papers will be peer reviewed on the basis of a full length manuscript and acceptance will be based on quality, originality and relevance. Accepted papers will be published in an electronic proceedings volume and be made available at the conference in CD-ROM. VENUE The conference will be held in the classic Casa Monica Hotel in St. Augustine Florida, the oldest city in the United States. A block of rooms has been reserved for the conference rate, and participants are encouraged to book them. Instructions will be posted in the website. St. Augustine is surrounded by beautiful beaches and is located 45 miles South of the Jacksonville International Airport, and 150 miles north of Orlando, its many attractions, and international airport. From gmsizemore2 from yahoo.com Fri Jan 9 18:09:25 2009 From: gmsizemore2 from yahoo.com (Glen M. Sizemore) Date: Fri Jan 9 22:52:45 2009 Subject: [Neuroscience] Re: SSRIs bind to post-synaptic 5-HT receptors and function as competitive antagonists? In-Reply-To: <0_ednaYTzJUf0vrUnZ2dnUVZ8srinZ2d@westnet.com.au> References: <49234c1f$0$26361$ed362ca5@nr5.newsreader.com> <4923e9c8$0$26332$ed362ca5@nr5.newsreader.com> <1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com> <4924ad7c$0$28062$ed362ca5@nr5.newsreader.com> <-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au> <49672529$0$24851$ed362ca5@nr5c.newsreader.com> <0_ednaYTzJUf0vrUnZ2dnUVZ8srinZ2d@westnet.com.au> Message-ID: <4967d93e$0$24851$ed362ca5@nr5c.newsreader.com> "John Hasenkam" wrote in message news:0_ednaYTzJUf0vrUnZ2dnUVZ8srinZ2d@westnet.com.au... > > 1. Recent controversy: > > I've just finished reading Prozac Backlash(2000) by Glenmullen, a Harvard > based psychiatrist who claims SSRIs carry all sorts of risks. There are > some risks involved but generally quite slight, though the issue of Redux > is worrying. It was an SSRI for appetite suppression but was found to > destroy serotonergic axons. GS: I had not heard about this, but I only follow such topics when the need arises. Strange that an SSRI would kill 5-HT neurons...by hyperstimulation? >Interesting given the known neurotoxicity of Ecstasy and that it is a >strong serotonin agonist. GS: Well...X is an indirect agonist - it is an uptake inhibitor (I don't know its specificity for serotonin, dopamine, and norepinephrine), and it probably does a lot of the things that amphetamines do in terms of release ("leaking") of monoamines directly from the cell. But there are a bunch of psychostimulatnts (other amphetamines included) that don't - as far as I know - lead to destruction of 5-HT neurons. Am I missing something? Are we on the same page here, John? >In addition recent studies on mice found that mice raised on prozac grow up >displaying depressive like symptoms. GS: It is easy - too easy! - to come up with a story here. Downregulation of the "5-HT system" could occur in a number of ways in response to hyperstimulation. Then, there is the whole issue of evaluating the cogency and quality of the behavioral studies you reference (I assume that you are referring to behavior here...if not...never mind!). >I think Glenmullen is way over the top but still have serious concerns >about the widespread use of SSRIs in children. I am not against >antidepressants, in fact I consider these drugs to be a great benefit, but >I have concerns about the excessive reliance on these drugs. Effexor can >induce serious withdrawal symptoms, I don't care what the authorities say >I've heard enough people describe their SSRI as a "security blanket" to >wonder if this is not a manifestation of dependency. In fact the general >advice now is that one should never abruptly stop taking these drugs >because of potential withdrawal problems. Whoops, that should read ... >because of a potential "antidepressant discontinuation syndrome". Ha! GS: I don't have much of an opinion on "whether or not anti-depressants actually work," but that does not mean that I am disinterested. The topic, quite frankly, overwhelms me. It overwhelms me because we are ultimately talking about complex human behavior and ALL of the conceptual issues that pertain when that is the subject matter under consideration. How much of what you read really appears to take these conceptual issues into consideration? Anyway...I have stressed this issue before...but I'm just ramblin' here. > > What is now being discovered is that CBT\psychotherapy is not only just as > effective in treating depression but appears to be much better at > preventing relapses. In fact SSRI's can only prevent relapses if one stays > on the drugs, which might explain why so many patients are on these for > life. Additionally, even strategies like insight meditation, exercise, and > dietary changes can be very helpful in dealing with depression. Even > vitamin D status may be of slight value because it inhibits > pro-inflammatory cytokine production. Then there is the Lancet study which > found slight increases in serotonin levels from sunshine exposure, this > probably relating to the changes in the melatonin - serotonin balance. Mt > is produced from serotonin, Mt production is rapidly stopped by sunlight > exposure(amacrine cells in retina, circadians, all that jazz), and Mt can > induce drowsiness and fatigue. That brings us to circadians, loss of > circadian stability is an intrinsic stressor, you can see the increase in > pro-inflammatory cytokines and for some depressives the loss of circadian > stability and hence sleep patterns is the straw that makes one rush for a > pill. Not surprising, even short periods of sleep deprivation can > significantly enhance the production of pro-inflammatory cytokines and > this has serious implications not just for depression but for cancer, > dementia, cardiovascular disease and what else??? The most remarkable > result I have read on the circadian issue was in relation to airline staff > who crossed timelines and experienced persistent circadian disruption but > without sleep deprivation. 5 year study found differences in temporal lobe > volumes and cognitive scores. Yes...you are simultaneously raising conceptual issues as well as alleged (not meant pejoratively) complex cascades of biochemical variables. I've already implied that I don't have much to offer - but I am interested in what you are saying. > > 2. > > I'm also wondering if the "competitive antagonist" = inverse agonist. > These ligands bind the receptor, change its conformation, and thereby > prevent second messenger\adaptor proteins coming into play when a agonist > ligand attaches to the receptor. GS: I don't know what you are referring to when you say " "these ligands." The difference between "competitive antagonists" (CAnt) and "inverse agonist" (IA) in my, admittedly, amateurish understanding, is that IAs reduce the basal level of spontaneous 2nd messanger stuff, as well as competing in the CAnt sense. >I haven't had time to look into this but the 5HT2c receptor appears to >activate production of arachidonic acid(need to find quantifiers for the >degree of production), a known pro-inflammatory mediator because it paves >the way for pge 2, which in turns helps maintain the expression of >pro-inflammatory cytokines(eg. il1, tnfa, il6 is tricky, can work both >ways). What is not that well known is that depression can involve >substantial increases in pro-inflammatory cytokines and it appears that >trying to understand depression by sole reference to the CNS is doomed to >fail. Keynote article: Cytokines and Depression: the need for a new >paradigm. I have this buried in my archives. We must consider endocrine and >immunological impacts as well. In regard to this Sapolsky et al has a great >review article, I need to read that again ... . The reason omega 3 intake >can help in depression, and possibly some other neuro disorders, is that >EPA inhibits A. acid production, diverting the pathways to >anti-inflammatory prostaglandins. What I have not looked into is how >serotonin impacts on immunological function, many immune cells have 5HT >receptors. > > For a very different perspective on these matters look up the ideas of > David Horrobin, I have a seminal article of his in my archives, that would > be a good starting point. If you so wish, give me some time, I'll email > you some of these articles. GS: This is all beyond my understanding. You're claiming that SSRIs work via some very roundabout mechanisms? I can't say...more power to you John. > > PS: haven't looked too closely at depression for many years now so I'm > rusty. I have a small mountain of data in my archives though so if you any > specific queries email me and I'll see what I can do to help. > > Be well, > > John. GS: Be well also, John. Trying to tackle so-called "psychiatric disorders" is a thankless task. I have talked about the conceptual problems that plague any discussion of complex human behavior, and you have alluded to potential biochemical issues that are independent of usual CNS considerations. And you have mentioned behavioral sorts of interventions. I simply don't have a strong opinion. I'm in an odd position...I think that our understanding of behavior (even in rats) is rudimentary, and any discussion of human "psychiatric disorders" is necessarily...errr...premature...yet...talk about them we must! Anyway...now I'm really rambling! Oh! Dang! I was going to give you a reference concerning SSRIs and direct 5-HT effects...I brought the damn paper home but can't find it right now! Anyway...I'll get it to you... G. From TASommer from gmail.com Fri Jan 9 21:14:48 2009 From: TASommer from gmail.com (Tim Sommer) Date: Fri Jan 9 22:52:51 2009 Subject: [Neuroscience] Joe LeDoux, Sensation and emotion, and more... Message-ID: <36e11e15-b3c1-46ea-8731-8779608db595@f18g2000vbf.googlegroups.com> Hey. My name is Tim -- I am involved with a group called THE SENSATION AND EMOTION NETWORK (www.sensationtoemotion.com). We support research in sensory processing and emotion regulation, and we are particularly interested in increasing awareness and finding solutions for Sensory Processing Disorders, a brain based problem that affects approximately five percent of school age children in the U.S. One subtype of SPD is Sensory Over Responsivity (SOR). SOR kids respond to sensory information (i.e. sound and touch) as though it were extremely aversive. They feel continually bombarded by stimuli. Patterns of instable moods are typical and SOR children find even pleasurable activities difficult, or unbearable. Awareness of SPD is very low. Children are frequently misdiagnosed, and the results can be devastating. On March 2 and 3 of this year, we are putting on The Sensation To Emotion Conference, which will bring together scholars, clinicians, and heavy in neuroscience, occupational therapy, music therapy, and related fields in order to advance the understanding of how sensory processing and emotion regulation interact, and how these processes affect human behavior. We will explore the neurobehavioral processes underlying the emotions often associated with a high reactivity level to sensory information, with attention focused on the auditory domains and upon the fear response. Since we greatly support an interdisciplinary approach, participants will include Joseph LeDoux, Lucy Miller, Jeffrey Brantley, Daniel Pine, Rosemary White, Elizabeth Phelps, Connie Tomaino, Peter Fonagy, Robert Zatorre, Gil Foley, and many more. For more information on the conference, please go to www.sensationtoemotion.com. From johnh from goawayplease.com Fri Jan 9 22:15:33 2009 From: johnh from goawayplease.com (John Hasenkam) Date: Sat Jan 10 12:34:26 2009 Subject: [Neuroscience] Re: SSRIs bind to post-synaptic 5-HT receptors andfunction as competitive antagonists? References: <49234c1f$0$26361$ed362ca5@nr5.newsreader.com><4923e9c8$0$26332$ed362ca5@nr5.newsreader.com><1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com><4924ad7c$0$28062$ed362ca5@nr5.newsreader.com><-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au><49672529$0$24851$ed362ca5@nr5c.newsreader.com><0_ednaYTzJUf0vrUnZ2dnUVZ8srinZ2d@westnet.com.au> Message-ID: In severe depression antidepressants are wonderful and vital. ECT can also provide remarkably fast and powerful benefits. ECT itself is a huge mystery, it can rapidly, within 24 hours, reduce depressive symptoms. Recently I came across a clue as to why: ECT rapidly boosts BDNF. BDNF is strongly implicated in depression. In my studies years ago I found a striking set of processes involving GABA, BDNF, il1, GCs, and NMDA in the hippocampus. A direct infusion of BDNF can also ameliorate depressive behavior in animal studies. This is very significant because in sustained major depression hippocampal atrophy can be very marked. There is also the suggestion that SSRIs boost neurogenesis and the processes I just mentioned also appear fundamental in promoting neurogenesis in the dentate gyrus, which provides neural progenitors to the hippocampus. As a general rule it appears that growth factors like BDNF tend to reduce inflammation, both processes appear to be mutually antagonistic. If I remember correctly SSRIs can reduce inflammation. It may be the case in severe depression that the SSRIs allow the reduction of inflammation to the extent that there is a resetting of neurotransmitter levels so allowing neurogenesis to recommence at stronger levels. Hence it can take some weeks for the effects to come through. Sapolsky argues that the hippocampal atrophy is arising from excessive glucocorticoid activation in the hippocampus. Interesting given that it was once thought that a biomarker for depression was the Dex suppression test. ie. depressives often have high levels of cortisol, which likes killing neurons. Over time high CORT can lead to glucocorticoid resistance. Thus, the inflammation suppressing effects of GCs are eliminated and so inflammation continues to rise, particularly given that ACTH and CRH can act as inflammatory mediators. So it is not that surprising that sustained major depression is also associated with increased risks for cancer, heart disease, and dementia. I must finish Katharine because my arms are getting really tired ... John. -- http://healthycuriousity.blogspot.com/ "KATHARINE LEAH DICKSON" wrote in message news:mailman.1364.1231531375.29717.neur-sci@net.bio.net... > I'm curious as to why SSRIs are most effective in the severely depressed - > at what point do antidepressants become more effective than talk therapy, > if indeed for all but the most extreme depressions CBT is more effective, > which seems to be the case? Is there a point where the neurochemical > milieu in the brain necessitates antidepressant intervening? > > Katharine Leah Dickson > kldickson@wisc.edu > > ----- Original Message ----- > From: John Hasenkam > Date: Friday, January 9, 2009 11:45 am > Subject: [Neuroscience] Re: SSRIs bind to post-synaptic 5-HT receptors and > function as competitive antagonists? > To: neur-sci@magpie.bio.indiana.edu > > >> 1. Recent controversy: >> >> I've just finished reading Prozac Backlash(2000) by Glenmullen, a >> Harvard >> based psychiatrist who claims SSRIs carry all sorts of risks. There >> are some >> risks involved but generally quite slight, though the issue of Redux >> is >> worrying. It was an SSRI for appetite suppression but was found to >> destroy >> serotonergic axons. Interesting given the known neurotoxicity of >> Ecstasy and >> that it is a strong serotonin agonist. In addition recent studies on >> mice >> found that mice raised on prozac grow up displaying depressive like >> symptoms. I think Glenmullen is way over the top but still have >> serious >> concerns about the widespread use of SSRIs in children. I am not >> against >> antidepressants, in fact I consider these drugs to be a great >> benefit, but I >> have concerns about the excessive reliance on these drugs. Effexor >> can >> induce serious withdrawal symptoms, I don't care what the authorities >> say >> I've heard enough people describe their SSRI as a "security blanket" >> to >> wonder if this is not a manifestation of dependency. In fact the >> general >> advice now is that one should never abruptly stop taking these drugs >> because >> of potential withdrawal problems. Whoops, that should read ... >> because of a >> potential "antidepressant discontinuation syndrome". Ha! >> >> >> What is now being discovered is that CBT\psychotherapy is not only >> just as >> effective in treating depression but appears to be much better at >> preventing >> relapses. In fact SSRI's can only prevent relapses if one stays on >> the >> drugs, which might explain why so many patients are on these for >> life. >> Additionally, even strategies like insight meditation, exercise, and >> dietary >> changes can be very helpful in dealing with depression. Even vitamin >> D >> status may be of slight value because it inhibits pro-inflammatory >> cytokine >> production. Then there is the Lancet study which found slight >> increases in >> serotonin levels from sunshine exposure, this probably relating to >> the >> changes in the melatonin - serotonin balance. Mt is produced from >> serotonin, >> Mt production is rapidly stopped by sunlight exposure(amacrine cells >> in >> retina, circadians, all that jazz), and Mt can induce drowsiness and >> >> fatigue. That brings us to circadians, loss of circadian stability is >> an >> intrinsic stressor, you can see the increase in pro-inflammatory >> cytokines >> and for some depressives the loss of circadian stability and hence >> sleep >> patterns is the straw that makes one rush for a pill. Not surprising, >> even >> short periods of sleep deprivation can significantly enhance the >> production >> of pro-inflammatory cytokines and this has serious implications not >> just for >> depression but for cancer, dementia, cardiovascular disease and what >> else??? >> The most remarkable result I have read on the circadian issue was in >> >> relation to airline staff who crossed timelines and experienced >> persistent >> circadian disruption but without sleep deprivation. 5 year study >> found >> differences in temporal lobe volumes and cognitive scores. >> >> 2. >> >> I'm also wondering if the "competitive antagonist" = inverse agonist. >> These >> ligands bind the receptor, change its conformation, and thereby >> prevent >> second messenger\adaptor proteins coming into play when a agonist >> ligand >> attaches to the receptor. I haven't had time to look into this but >> the 5HT2c >> receptor appears to activate production of arachidonic acid(need to >> find >> quantifiers for the degree of production), a known pro-inflammatory >> mediator >> because it paves the way for pge 2, which in turns helps maintain the >> >> expression of pro-inflammatory cytokines(eg. il1, tnfa, il6 is >> tricky, can >> work both ways). What is not that well known is that depression can >> involve >> substantial increases in pro-inflammatory cytokines and it appears >> that >> trying to understand depression by sole reference to the CNS is >> doomed to >> fail. Keynote article: Cytokines and Depression: the need for a new >> paradigm. I have this buried in my archives. We must consider >> endocrine and >> immunological impacts as well. In regard to this Sapolsky et al has a >> great >> review article, I need to read that again ... . The reason omega 3 >> intake >> can help in depression, and possibly some other neuro disorders, is >> that EPA >> inhibits A. acid production, diverting the pathways to >> anti-inflammatory >> prostaglandins. What I have not looked into is how serotonin impacts >> on >> immunological function, many immune cells have 5HT receptors. >> >> For a very different perspective on these matters look up the ideas >> of David >> Horrobin, I have a seminal article of his in my archives, that would >> be a >> good starting point. If you so wish, give me some time, I'll email >> you some >> of these articles. >> >> PS: haven't looked too closely at depression for many years now so >> I'm >> rusty. I have a small mountain of data in my archives though so if >> you any >> specific queries email me and I'll see what I can do to help. >> >> Be well, >> >> John. >> >> "How many economists does it take to change a lightbulb? >> None, the invisible hand will do it." >> >> Citation: Mean markets and Lizard Brains. >> >> >> >> >> >> "Glen M. Sizemore" wrote in message >> news:49672529$0$24851$ed362ca5@nr5c.newsreader.com... >> > >> > "John Hasenkam" wrote in message >> > news:-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au... >> >> Hey Glen, >> >> >> >> Would you mind posting your provisional answer? Depression is a >> hobby >> >> horse of mine and given recent controversy over just how SSRIs do >> what >> >> they do I'm interested. >> >> >> >> Trust the musical marvel is doing well. >> >> >> >> >> >> John. >> > >> > Hi John, >> > I am trying to get to the bottom of this alleged binding of some >> SSRIs to >> > the 5-HT2c receptor - I may have spoken too soon! I'll get back to >> you on >> > this. I am going to have to become educated on this topic since I >> am going >> > to be involved in the pre-clinical anti-depressant business. What >> are you >> > referring to when you talk about the "recent controversy"? >> > >> > Yes, Mike is doing well - he's become sort of good on the sax (just >> a >> > hobby though). He went to see Perlman the other night - he was >> supposed to >> > get to meet him before the performance, but Perlman was not up to >> meeting >> > people. Mike spends a lot of time watching Perlman and old tapes of >> >> > Heifetz - that's in between times when he is teaching himself to >> play >> > drums along with an old Little Feat LP we have. >> > >> > Hope you are well. >> > >> > Regards, >> > Glen >> > >> > >> >> >> >> >> >>> I can now answer my own question, but I'll post the provisional >> answer >> >>> for those that might be interested, and I'll provide a reference >> for >> >>> those that are interested. Some SSRIs do, indeed, bind at the >> 5-HT2c >> >>> receptor, and function as competitive antagonists. >> >> >> >> >> >> >> >> "Glen M. Sizemore" wrote in message >> >> news:4924ad7c$0$28062$ed362ca5@nr5.newsreader.com... >> >>> >> >>> "r norman" wrote in message >> >>> news:1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com... >> >>>> On Wed, 19 Nov 2008 05:26:55 -0500, "Glen M. Sizemore" >> >>>> wrote: >> >>>> >> >>>>> >> >>>>>"Glen M. Sizemore" wrote in message >> >>>>>news:49234c1f$0$26361$ed362ca5@nr5.newsreader.com... >> >>>>>> Someone I know claims that SSRIs bind at post-synaptic serotonin >> >>>>>> receptors, and function as competitive antagonists. Anyone >> know >> >>>>>> anything >> >>>>>> about this? Thanks ahead of time... >> >>>>>> >> >>>>>> G. >> >>>>> >> >>>>>Correction: SOME SSRIs >> >>>> >> >>>> Could (s)he be thinking of the action of pindolol which is >> sometimes >> >>>> used in conjunction with SSRIs? >> >>> >> >>> Hi Dr. Norman, >> >>> >> >>> I can now answer my own question, but I'll post the provisional >> answer >> >>> for those that might be interested, and I'll provide a reference >> for >> >>> those that are interested. Some SSRIs do, indeed, bind at the >> 5-HT2c >> >>> receptor, and function as competitive antagonists. >> >>> >> >>> Cordially, >> >>> Glen >> >> >> >> >> > >> >> >> _______________________________________________ >> Neur-sci mailing list >> Neur-sci@net.bio.net >> http://www.bio.net/biomail/listinfo/neur-sci >> > From johnh from goawayplease.com Sat Jan 10 00:27:29 2009 From: johnh from goawayplease.com (John Hasenkam) Date: Sat Jan 10 12:34:37 2009 Subject: [Neuroscience] Re: SSRIs bind to post-synaptic 5-HT receptors and function as competitive antagonists? References: <49234c1f$0$26361$ed362ca5@nr5.newsreader.com> <4923e9c8$0$26332$ed362ca5@nr5.newsreader.com> <1f38i4ptqiifib4vmg6d6elrrm30t0t6s0@4ax.com> <4924ad7c$0$28062$ed362ca5@nr5.newsreader.com> <-f-dnT--Crq0jPvUnZ2dnUVZ8tPinZ2d@westnet.com.au> <49672529$0$24851$ed362ca5@nr5c.newsreader.com> <0_ednaYTzJUf0vrUnZ2dnUVZ8srinZ2d@westnet.com.au> <4967d93e$0$24851$ed362ca5@nr5c.newsreader.com> Message-ID: "Glen M. Sizemore" wrote in message news:4967d93e$0$24851$ed362ca5@nr5c.newsreader.com... > > "John Hasenkam" wrote in message > news:0_ednaYTzJUf0vrUnZ2dnUVZ8srinZ2d@westnet.com.au... >> >> 1. Recent controversy: >> >> I've just finished reading Prozac Backlash(2000) by Glenmullen, a Harvard >> based psychiatrist who claims SSRIs carry all sorts of risks. There are >> some risks involved but generally quite slight, though the issue of Redux >> is worrying. It was an SSRI for appetite suppression but was found to >> destroy serotonergic axons. > > GS: I had not heard about this, but I only follow such topics when the > need > arises. Strange that an SSRI would kill 5-HT neurons...by > hyperstimulation? JH: Hyper stimulation is posited as a cause. However just a few days ago I came across this: J Neurochem. 1997 Nov;69(5):2096-101. Serotonin acts as a radical scavenger and is oxidized to a dimer during the respiratory burst of activated microglia. Department of Psychiatry, University of Göttingen, Germany. Serotonin (5-HT) is known to be readily oxidized and to act as a scavenger of reactive oxygen species produced, e.g., in the presence of peroxidase and H2O2 or during the respiratory burst of phagocytes. One major oxidation product formed under these conditions, the 5-HT dimer 5,5'-dihydroxy-4,4'-bitryptamine (DHBT), was suggested to have neurotoxic properties and to contribute to neuronal damage in neurodegenerative disorders. It is shown in the present study that the luminol-enhanced chemiluminescence signal measured after stimulation of the respiratory burst activity of cultivated rat microglial cells by the addition of phorbol 12-myristate 13-acetate is suppressed by 5-HT in a dose-dependent manner. During this process, 5-HT is oxidized to DHBT. Neither the intraventricular injection of DHBT nor the addition of DHBT to cultured astrocytes, neurons, or PC-12 cells was found to cause measurable cytotoxic effects. It is concluded that extracellular 5-HT locally released from platelets and 5-HT nerve endings at sites of brain damage or inflammation, through its suppressant effect on the release of reactive oxygen species during the respiratory burst of activated microglia, may contribute to attenuate secondary tissue damage in the CNS. PMID: 9349555 [PubMed - indexed for MEDLINE] >>Interesting given the known neurotoxicity of Ecstasy and that it is a >>strong serotonin agonist. > > GS: Well...X is an indirect agonist - it is an uptake inhibitor (I don't > know its specificity for serotonin, dopamine, and norepinephrine), and it > probably does a lot of the things that amphetamines do in terms of release > ("leaking") of monoamines directly from the cell. But there are a bunch > of > psychostimulatnts (other amphetamines included) that don't - as far as I > know - lead to destruction of 5-HT neurons. Am I missing something? Are we > on the same page here, John? JH: Uptake inhibitor, the typical strategy. Not sure about serotonin but it is known that MAOs which degrade dopamine create products which are neurotoxic. Hence agents like selegiline can be neuroprotective because of their inhibition of MAOs. So it might be interesting to see what degradation products arise from the reuptake of serotonin. >>In addition recent studies on mice found that mice raised on prozac grow >>up >>displaying depressive like symptoms. > > GS: It is easy - too easy! - to come up with a story here. Downregulation > of > the "5-HT system" could occur in a number of ways in response to > hyperstimulation. Then, there is the whole issue of evaluating the cogency > and quality of the behavioral studies you reference (I assume that you are > referring to behavior here...if not...never mind!). That's the problem: too easy. Mencken: "For every human problem, there is a neat, simple solution; and it is always wrong" See: http://www.webmd.com/baby/news/20041026/early-exposure-to-prozac-may-up-anxiety-risk and Brain Res. 2000 Nov 17;883(2):205-15. Chronic fluoxetine administration to juvenile rats prevents age-associated dendritic spine proliferation in hippocampus. Norrholm SD, Ouimet CC. Program in Neuroscience, Department of Psychology, Florida State University, 211 Biomedical Research Facility, Tallahassee, FL 32306-4340, USA. The density of dendritic spines, the postsynaptic sites of most excitatory synapses, increases during the first 2 postnatal months in rat hippocampus. Significant alterations in hippocampal levels of serotonin and norepinephrine impact synaptic development during this time period. In the present study, dendritic spine density was studied in the hippocampus (CA1) and dentate gyrus of juvenile rats acutely and chronically exposed to antidepressant drugs that act on serotonin and norepinephrine. One group of 21-day-old rats was given a single injection of a serotonin specific re-uptake inhibitor (fluoxetine or fluvoxamine), a norepinephrine-specific re-uptake inhibitor (desipramine), or saline and killed after 24 h. A second group of rats was injected daily, beginning on postnatal day (PN) 21, for 3 weeks. This group was further subdivided into rats that were killed 1 day or 21 days after the last injection. Golgi analysis showed that a single injection of fluvoxamine produced a significant increase in dendritic spine density in stratum radiatum of CA1 and in the dentate gyrus. Further, acute treatment with all three antidepressants increased the total length of secondary dendrites in CA1, with fluoxetine and desipramine increasing the number of secondary dendrites as well. In fluoxetine-treated animals killed on days 42 or 62 (1 or 21 days post-treatment, respectively), dendritic spine density remained at levels present in CA1 at 21 days. These results show that acute antidepressant treatment can impact dendritic length and spine density, and raise the possibility that chronic fluoxetine treatment arrests spine development into young adulthood. PMID: 11074049 [PubMed - indexed for MEDLINE] The above paper is interesting because a great many patients on SSRIs develop tolerance. One hopes this tolerance is arising because of "neural adjustments" rather than pathology. I can't evaluate the behavioral studies Glen, lack the skills for that. > >>I think Glenmullen is way over the top but still have serious concerns >>about the widespread use of SSRIs in children. I am not against >>antidepressants, in fact I consider these drugs to be a great benefit, but >>I have concerns about the excessive reliance on these drugs. Effexor can >>induce serious withdrawal symptoms, I don't care what the authorities say >>I've heard enough people describe their SSRI as a "security blanket" to >>wonder if this is not a manifestation of dependency. In fact the general >>advice now is that one should never abruptly stop taking these drugs >>because of potential withdrawal problems. Whoops, that should read ... >>because of a potential "antidepressant discontinuation syndrome". Ha! > > GS: I don't have much of an opinion on "whether or not anti-depressants > actually work," but that does not mean that I am disinterested. The topic, > quite frankly, overwhelms me. It overwhelms me because we are ultimately > talking about complex human behavior and ALL of the conceptual issues that > pertain when that is the subject matter under consideration. How much of > what you read really appears to take these conceptual issues into > consideration? Anyway...I have stressed this issue before...but I'm just > ramblin' here. JH: The drugs work but then so does exercise, ECT ... . Finding a "final common pathway" is the challenge for many but I suspect that this is an error. There may be several final common pathways that can instantiate depression. Good, you're overwhelmed. Anyone who looks at this closely and isn't overwhelmed is either an idiot or a liar. Before my vision collapsed several years ago I was putting a lot of work into this. Very depressing and as the doctors advised me: you have a very complex neuro-ophthalamic pathology so stop reading so much. Stuff ém, they were wrong. I threw a lot of data at you to demonstrate the sheer complexity of this matter. If you come at it piecemeal it won't make sense and never will. You will need to establish a broad physiological framework and that takes lots of work. That's why I mentioned the papers by Sapolsky and Horrobin. Been there, done that, and it still don't make sense to me. Behavior: There are too many conceptual mindfields. There is the problem diagnosing depression, a lack of reliable biomarkers for depression, the need to exclude subjects carrying an allele for the 5HT transporter which, together with early childhood neglect and present stress, markedly increases the risk of depression. Consideration should also be given to tryptophan absorption and intake as it is a necessary precursor for serotonin production. Even the levels of IDO, which diverts tryptophan metabolism towards Ky. Acid instead of serotonin production, is important. For example, think of "sickness behavior"". Immune cells release IDO as many bacteria require serotonin. The downside is loss of serotonin production. At a guess I suggest pro-inflammatory cytokines increase the expression of IDO. Don't know if microglia express IDO. >> >> What is now being discovered is that CBT\psychotherapy is not only just >> as >> effective in treating depression but appears to be much better at >> preventing relapses. In fact SSRI's can only prevent relapses if one >> stays >> on the drugs, which might explain why so many patients are on these for >> life. Additionally, even strategies like insight meditation, exercise, >> and >> dietary changes can be very helpful in dealing with depression. Even >> vitamin D status may be of slight value because it inhibits >> pro-inflammatory cytokine production. Then there is the Lancet study >> which >> found slight increases in serotonin levels from sunshine exposure, this >> probably relating to the changes in the melatonin - serotonin balance. Mt >> is produced from serotonin, Mt production is rapidly stopped by sunlight >> exposure(amacrine cells in retina, circadians, all that jazz), and Mt can >> induce drowsiness and fatigue. That brings us to circadians, loss of >> circadian stability is an intrinsic stressor, you can see the increase in >> pro-inflammatory cytokines and for some depressives the loss of circadian >> stability and hence sleep patterns is the straw that makes one rush for a >> pill. Not surprising, even short periods of sleep deprivation can >> significantly enhance the production of pro-inflammatory cytokines and >> this has serious implications not just for depression but for cancer, >> dementia, cardiovascular disease and what else??? The most remarkable >> result I have read on the circadian issue was in relation to airline >> staff >> who crossed timelines and experienced persistent circadian disruption but >> without sleep deprivation. 5 year study found differences in temporal >> lobe >> volumes and cognitive scores. > > Yes...you are simultaneously raising conceptual issues as well as alleged > (not meant pejoratively) complex cascades of biochemical variables. I've > already implied that I don't have much to offer - but I am interested in > what you are saying. >> 2. >> >> I'm also wondering if the "competitive antagonist" = inverse agonist. >> These ligands bind the receptor, change its conformation, and thereby >> prevent second messenger\adaptor proteins coming into play when a agonist >> ligand attaches to the receptor. > > GS: I don't know what you are referring to when you say " "these ligands." > The difference between "competitive antagonists" (CAnt) and "inverse > agonist" (IA) in my, admittedly, amateurish understanding, is that IAs > reduce the basal level of spontaneous 2nd messanger stuff, as well as > competing in the CAnt sense. JH: This might help(full paper freely available at the link): http://pharmrev.aspetjournals.org/cgi/content/abstract/57/2/147 Multiple Signaling States of G-Protein-Coupled Receptors Abstract--Studies have been amassed in the past several years indicating that an agonist can conform a receptor into an activation state that is dependent upon an intrinsic property of the agonist usually based upon its chemical composition. Theoretically, each different agonist could impart its own unique activation state. Evidence for multiple signaling states for the G-protein-coupled receptors will be reviewed and is derived from many different pharmacological behaviors: efficacy, kinetics, protean agonism, differential desensitization and internalization, inverse agonism, and fusion chimeras. A recent extension of the ternary complex model is suggested by evidence that the different processes that govern deactivation, such as desensitization and internalization, is also regulated by conformers specific to the agonist. Rhodopsin may serve as a primer for the study of multiple activation states. Therapeutic implications that utilize multiple signaling states hold vast promise in the rationale design of drugs. .... Structural changes induced by the binding of agonists, antagonists, and inverse agonists to the cloned -opioid receptor immobilized on a solid-supported lipid bilayer were also investigated using plasmon-waveguide resonance spectroscopy. Agonist binding causes an increase in membrane thickness because of receptor elongation, a mass density increase due to an influx of lipid molecules into the bilayer, and an increase in refractive index anisotropy due to transmembrane helix and fatty acyl chain ordering. In contrast, antagonist binding produces no measurable change in either membrane thickness or mass density and a significantly larger increase in refractive index anisotropy, the latter thought to be due to a greater extent of helix and acyl chain ordering within the membrane interior. An inverse agonist produces membrane thickness, mass density, and refractive index anisotropy increases which are similar to, but considerably smaller than, those generated by agonists ... 1. Native Systems. Interesting and novel ligands exist called "protean" agonists. Proteus was a sea god in Greek mythology and the herdsman of Poseidon's seals who had the ability to change his shape at will. Protean agonists were predicted to exist from theoretical arguments based upon multiple active conformations of GPCRs (Kenakin, 1997). It was predicted that a protean agonist could act both as an agonist or an inverse agonist at the same GPCR. To see this effect, one has to use receptors or tissues that exhibit a high level of constitutive activity. The reversal from agonism to inverse agonism would only occur when an agonist produces an active conformation of lower efficacy than a totally active conformation. Therefore, the higher the constitutive activity, the greater chance to see this other conformation. Gbahou et al. (2003) showed that proxyfan, a high-affinity histamine H3-receptor ligand, acted as a protean agonist at recombinant H3 receptors expressed in the Chinese hamster ovary cells. Using neurochemical and behavioral assays in rodents and cats, proxyfan displayed a spectrum of activity ranging from full agonism to full inverse agonism. Thus, protean agonism demonstrated the existence of alternative agonist active states that was different from the constitutively active state in this system. This was the first report of protean agonism existing for native receptors under physiological conditions. >>I haven't had time to look into this but the 5HT2c receptor appears to >>activate production of arachidonic acid(need to find quantifiers for the >>degree of production), a known pro-inflammatory mediator because it paves >>the way for pge 2, which in turns helps maintain the expression of >>pro-inflammatory cytokines(eg. il1, tnfa, il6 is tricky, can work both >>ways). What is not that well known is that depression can involve >>substantial increases in pro-inflammatory cytokines and it appears that >>trying to understand depression by sole reference to the CNS is doomed to >>fail. Keynote article: Cytokines and Depression: the need for a new >>paradigm. I have this buried in my archives. We must consider endocrine >>and >>immunological impacts as well. In regard to this Sapolsky et al has a >>great >>review article, I need to read that again ... . The reason omega 3 intake >>can help in depression, and possibly some other neuro disorders, is that >>EPA inhibits A. acid production, diverting the pathways to >>anti-inflammatory prostaglandins. What I have not looked into is how >>serotonin impacts on immunological function, many immune cells have 5HT >>receptors. >> >> For a very different perspective on these matters look up the ideas of >> David Horrobin, I have a seminal article of his in my archives, that >> would >> be a good starting point. If you so wish, give me some time, I'll email >> you some of these articles. > > GS: This is all beyond my understanding. You're claiming that SSRIs work > via > some very roundabout mechanisms? I can't say...more power to you John. JH: I'm saying that there are multiple processes involved and I don't have a clue as to how to make sense of it all. I don't doubt there will be direct and indirect effects. Depression can arise through a number of avenues, whether or not we can ever define depression within individuals by reference to a specific physiological and neurological status is a question I can't answer. That is, in any given individual we may define depression by a set of states but we should not assume that the same physiological status will result in depression in other individuals. Yeah, that seems odd. The other issue here is that we must consider all the types of depression: Major dysthymia post partum(I'll take odds that relates to omega 3 stripping by the fetus from the mother-does happen - and increase in IDO) bipolar sickness behavior reactive 5HT transporter induced tryptophan depletion induced SAD >> >> PS: haven't looked too closely at depression for many years now so I'm >> rusty. I have a small mountain of data in my archives though so if you >> any >> specific queries email me and I'll see what I can do to help. >> >> Be well, >> >> John. > > GS: Be well also, John. Trying to tackle so-called "psychiatric disorders" > is a thankless task. I have talked about the conceptual problems that > plague > any discussion of complex human behavior, and you have alluded to > potential > biochemical issues that are independent of usual CNS considerations. And > you > have mentioned behavioral sorts of interventions. I simply don't have a > strong opinion. I'm in an odd position...I think that our understanding of > behavior (even in rats) is rudimentary, and any discussion of human > "psychiatric disorders" is necessarily...errr...premature...yet...talk > about > them we must! Anyway...now I'm really rambling! Oh! Dang! I was going to > give you a reference concerning SSRIs and direct 5-HT effects...I brought > the damn paper home but can't find it right now! Anyway...I'll get it to > you... JH: Disgusting personal example. Because of my vision problem I was referred to the Commonwealth Rehabilitation Service some years ago. The "psychologist" there was convinced I had a psychopathology, insisted on a psychiatric assessment. The two major problems the psychiatrist identified were: "Of course there were the prejudices and biases that happened such that most people on seeing his appearance would regard him as mentally deficient, retarded and more likely to make unfavourable conclusions about his personality and character, this of course is well accepted and well substantiated in the literature. One only needs to look at the beauty and cosmetic surgery industry to confirm society's preoccupation with youth and beauty. .... When asked directly about his self-esteem he rejected the concept outright and gave an academic argument and justification for his opinion, through which one can see insight into his personality and intelligence. Therein lies another aspect of this man's presentation and that is indeed his personality. Without having formal testing I don't believe there is any evidence to say that he has an organic personality problem, nevertheless he is an unusual character. His appearance belies his higher intelligence and indeed substantial knowledge base. I suspect at times he is able in his words to 'play dumb' and then catch people out if not embarrass and humiliate them with his intellectual prowess." --------- I will never forget the look on his face when I shot him down over the self-esteem question. He didn't even bother to challenge me, probably because he knew I was right and he felt a little foolish for asking a question based on a spurious assumption(look up "Roy Baumeister" http://www.fsu.edu/profiles/baumeister/). Incredibly, the psychiatrist was quietly suggesting that the psychologist's opinion of me was potentially driven by the types of discrimination people like myself are often victims of. And yet, the "psychologist" then wanted another assessment because she thought the first was in error. I wish more clinicians shared your cynicism. I don't know why you consider your position "odd". Perhaps because of a general lack of cynicism? Cynicism is a euphemism for realism. Seeing things the way they really are, instead of the way we'd like them to be. *Hans Selye For all this rambling, I haven't even addressed why SNRI's may be a better strategy, particularly given that nore may inhibit microglial activation and by increasing activity in the orbitofrontal cortices(particularly the right as nore expression is higher in the right frontals) and these corticies are believed to inhibit amygdala activity. There is the suggestion that in depressives the right amygdala is larger than in norms. I'm just throwing stuff at you Glen in the hope that it will give you some idea of what you have let yourself in for. At an epistemological level you have a very difficult choice: to focus solely on the neurobiology of antidepressants or attempt to develop a broader perspective on the issue of depression. If I may presume to be directive, I suggest you focus on the former and play with the latter. Congratulations, you made me open a long dormant database. > G. > begin 666 delta.gif M1TE&.#EA!@`+`,(``````"0D)$E)26UM;9*2DK:VMMO;V____R'Y! $```<` M+ `````&``L`0 ,@>!IC0*<,%4&AC8(XS[#401A"1P04,:Q'`!6"-P7&D0`` !.P`` ` end begin 666 fig-down.gif M1TE&.#=A" `'`( ``/___P```"P`````" `'`$ "#(2/H8&@#<^3:QI;```[ ` end From tehgabriel from web.de Wed Jan 14 06:04:36 2009 From: tehgabriel from web.de (Tom) Date: Wed Jan 14 14:20:21 2009 Subject: [Neuroscience] Problems with transfection: eGFP - mCherry interactions? Message-ID: <5cbe281f-abe6-467e-8bd3-3a89110b317d@z6g2000pre.googlegroups.com> Hi! Did anybody ever tried co-expression of eGFP and mCherry in cultured hippocampal neurons? I tried this now repeatedly using CaPhos- and lipofectamine protocols but i never found a nice red fluroescence. No problems occured when i co-transfected eGFP and mRFP or with singel transfection of just mCherry. Now why won't the eGFP/mCherry co-transfection work? Thanks for comments! Regards, Thomas From michael.schrey from t-online.de Wed Jan 14 06:41:26 2009 From: michael.schrey from t-online.de (Michael Schrey) Date: Wed Jan 14 14:20:27 2009 Subject: [Neuroscience] Re: Ion channel distributions In-Reply-To: <44e366f0-a97b-492f-a9fc-1f29a0636d1b@x16g2000prn.googlegroups.com> References: <44e366f0-a97b-492f-a9fc-1f29a0636d1b@x16g2000prn.googlegroups.com> Message-ID: Hello Rick, ad (1): - no. Neither concerning type of channel (gating mechanism, ion permeablility, "speed"), nor concerning tissue type (neurons vs. muscle for example), nor concerning distribution in one cell (axons vs. soma, Ranvier's vs. myelin sheath). ad (2): - kind of yes, but: rarely is one type of channel (isoform) representative for only one type of cell ad (3): - probably not, as ionchannel-distribution is one way of "specializing" in cells, which occurs as well in vertebrates as in invertebrates. For a quite comprehensive overview on sodium channels see Goldin, A. L. (1999) Diversity of mammalian voltage-gated sodium channels. Ann N Y Acad Sci 868, 38-50. Goldin, A. L. (2001) Resurgence of sodium channel research. Annu Rev Physiol 63, 871-894. Or have a look at my (German) thesis at http://deposit.ddb.de/cgi-bin/dokserv?idn=982011482&dok_var=d1&dok_ext=pdf&filename=982011482.pdf Good luck with your project! Michael Rick Giuly schrieb: > Hello All, > > I'm interested in modeling neurons and I have a few questions: > > (1) In adult animals, are ion channel distributions constant? > > (2) Do particular cell types have well defined ion channel > distributions that are similar among all cells of the type? (For > example does a Purkinje cell have a predictable ion channel > distribution?) > > (3) Are the answers to questions (1) and (2) different for vertebrates > and invertebrates? > > Any comments or paper recommendations are appreciated. I've done some > literature searching and found some fragments of information on these > topics but nothing definitive yet. > > -Rick From connelly.bill from gmail.com Thu Jan 15 04:01:28 2009 From: connelly.bill from gmail.com (Bill) Date: Thu Jan 15 10:22:07 2009 Subject: [Neuroscience] Decay constants. What does "weighted" mean? Message-ID: <86e1f737-b55f-4a73-92ee-a59c102d426a@y1g2000pra.googlegroups.com> Hi, Synaptic events decay with an (bi)exponetial function. You can of course report the decay constant, which I understand, but what do people mean when they refer to the weighted decay constant? Thanks. From johnh from goawayplease.com Thu Jan 15 11:00:29 2009 From: johnh from goawayplease.com (John Hasenkam) Date: Thu Jan 15 11:55:15 2009 Subject: [Neuroscience] Re: "cerebral encephalitis" residual effects References: Message-ID: Residual effects should be expected but it is impossible to know the extent and nature of these effects. Even chemotherapy in childhood can have long lasting effects on brain function and behavior. Your cousin has experienced two distinct kinds of brain trauma: one from the infection and a milder form arising from the immune response to that infection. He may well be sensitised to psychological stress and so be more prone to depression and behavior issues arising from stressful events. He may also experience sleep problems and have to put in much more effort to sustain concentration, with subsequent tiring much earlier than other people. You could go looking for sites of damage and probably find something. However the value of this is problematic and the damage may well be diffuse and difficult to establish. That is, to clearly establish evidence of brain damage could require some rather esoteric imaging technologies and even if the same is established it won't necessarily bring forth any therapeutic possibilities. For eg. the Amen Clinics site mentions SPECT imaging. Drugs? What drugs? Yes, there may be some value but it really depends on the types of drugs and the targets for those drugs. There may be some nutritional and behavior interventions that can help but you'll need to find a damned good clinician who is prepared to put in a lot of work. Of course that means dollars, time, and commitment. A quick look at the Amen Clinics site at least suggests he knows what he is on about but the title of one of his publications: "magnificient mind at any age" is ringing alarm bells in my head. Too much hyperbole. The website also offers a number of products they are selling with fancy names and mediocre contents. For example, want to boost omega 3s? Oh I don't know, you could buy those fancy pills or eat more Atlantic or Tasmanian salmon. "Neuro St. Wort" as a product. Oh please ... . St. John's Wort is a regular and proven treatment for mild to moderate depression, very widely used in Europe. Neurolink: Vitamin B6. Or you could eat more leafy greens. L-tyrosine: essential amino acid for dopamine and nore creation. Not a bad idea but could be problematic with dopamine agonists or SNRIs(?). Brain injury can lead to a chronically lowered "dopamine tone" so L-tyrosine may help to address this; if it exists in your cousin(lethargy, easily tired, poor attentional skills). GABA: inhibitory neurotransmitter, a nice settling effect but how much sedation do you want in a developing brain? Inositol: Vitamin B group: eat more greens. Taurine: Good idea. 5HTP: serotonin. Whoopee. --- Let me guess what will happen here. You go to the clinic, the doctor, probably with the best of intentions, will advise this supplements and that supplement ... . I also suspect he has a MRI machine so will want to use that as often as possible. The acid test for these "revolutionary approaches" cannot be established by those promoting these approaches. You need to find independent appraisals of what Amen is offering. You don't determine the value of a product by the claims of the seller, a lesson too many people forget when addressing medical issues. Who? Me? Cynical? Always be cynical of celebrity doctors. What can you do? Maximise the child's overall health, particularly nutrition wise. Long list here. Address specific behavior issues with a good therapist, which can be hard to find. Consider stress management programs. ---- I could run off a list of supplements that might help but I've got nothing to sell. You might be able to find good therapists through your regular doctor or a brain injury organisation. --- Yes, drugs can be very useful but it can take quite a bit of experimentation to find the right drugs and doses. John. -- http://healthycuriousity.blogspot.com/ "JR" wrote in message news:Xns9B9172F17A03842437q4qu2329292343@0.0.0.1... > Have a cousin who had "cerebral encephalitis" as an infant. > > Had to learn to walk a second time; problems with spatial abilities, motor > skills,conduct problems as a kid. > > Are there any patterns/locations of damage that typically occur in such > cases? > > How valid is Daniel Amen's techniques and would the be useful in such a > case? > > Can neuropsychologists really determine the location of brain damage? > > Do drugs really offer any solution in these cases? > > Any answers? Thanks. From r_s_norman from _comcast.net Thu Jan 15 11:17:00 2009 From: r_s_norman from _comcast.net (r norman) Date: Thu Jan 15 11:55:21 2009 Subject: [Neuroscience] Re: Decay constants. What does "weighted" mean? References: <86e1f737-b55f-4a73-92ee-a59c102d426a@y1g2000pra.googlegroups.com> Message-ID: <0tnum4hfq9q5s3glfjsts7acf15u3rkdnf@4ax.com> On Thu, 15 Jan 2009 01:01:28 -0800 (PST), Bill wrote: >Hi, > >Synaptic events decay with an (bi)exponetial function. You can of >course report the decay constant, which I understand, but what do >people mean when they refer to the weighted decay constant? > >Thanks. When a function does not show simple exponential decay, but rather has several terms each with a different time constant, then each term has a "weight" associated with it a exp(-t/t1) + b exp(-t/t2) where t1 and t2 are two time constants and a and b are the respective "weights". That is the usual meaning, but describe the use of the term in context, or better, the citation with a material and methods sections talking about how to calculate the values, and I can describe it better. Note: an RC circuit, of course, has a simple exponential decay but synaptic decay is complicated because of the spatial decay superimposed on the temporal decay. That is, the partial differential equation of the cable equation of the dendritic tree is rather different from the simple differential equation of an RC circuit. Of course, lingering synaptic activation also can complicate the decay pattern. That means that synaptic decay is not simple exponential decay. From I.Vida from bio.gla.ac.uk Thu Jan 15 12:40:10 2009 From: I.Vida from bio.gla.ac.uk (Imre Vida) Date: Thu Jan 15 17:00:57 2009 Subject: [Neuroscience] Re: Decay constants. What does "weighted" mean? In-Reply-To: <0tnum4hfq9q5s3glfjsts7acf15u3rkdnf@4ax.com> References: <86e1f737-b55f-4a73-92ee-a59c102d426a@y1g2000pra.googlegroups.com> <0tnum4hfq9q5s3glfjsts7acf15u3rkdnf@4ax.com> Message-ID: <20090115174010.GH3278@bio.gla.ac.uk> On Thu, Jan 15, 2009 at 09:17:00AM -0700, r norman wrote: > On Thu, 15 Jan 2009 01:01:28 -0800 (PST), Bill > wrote: > > >Hi, > > > >Synaptic events decay with an (bi)exponetial function. You can of > >course report the decay constant, which I understand, but what do > >people mean when they refer to the weighted decay constant? > > > >Thanks. > > When a function does not show simple exponential decay, but rather has > several terms each with a different time constant, then each term has > a "weight" associated with it > a exp(-t/t1) + b exp(-t/t2) > where t1 and t2 are two time constants and a and b are the respective > "weights". from this, the weighted decay time constant is: tw = (a*t1+b*t2)/(a+b) it is a simplification, to describe the "speed" of the decay with a single value and enable the comparison of "events" with different decay kinetics i guess when you say synaptic events, you mean E/IPSCs i.e. currents. Their decay kinetics is dependent on when the channels close, deactivate or desensitize. imre > That is the usual meaning, but describe the use of the term in > context, or better, the citation with a material and methods sections > talking about how to calculate the values, and I can describe it > better. > > Note: an RC circuit, of course, has a simple exponential decay but > synaptic decay is complicated because of the spatial decay > superimposed on the temporal decay. That is, the partial differential > equation of the cable equation of the dendritic tree is rather > different from the simple differential equation of an RC circuit. Of > course, lingering synaptic activation also can complicate the decay > pattern. That means that synaptic decay is not simple exponential > decay. > > > > _______________________________________________ > Neur-sci mailing list > Neur-sci@net.bio.net > http://www.bio.net/biomail/listinfo/neur-sci From t.lewis from unsw.edu.au Thu Jan 15 17:46:53 2009 From: t.lewis from unsw.edu.au (Trevor Lewis) Date: Thu Jan 15 20:01:56 2009 Subject: [Neuroscience] Re: Decay constants. What does "weighted" mean? Message-ID: <7ha0n3$4r6k6@INFPACM003.services.comms.unsw.edu.au> Dear Bill, A little more information to add to what r norman posted: As explained, for a response that can be fitted with the sum of two exponentials - f(t) = a exp(-t/t1) + b exp(-t/t2) where t1 and t2 are the time constants and a and b are the initial amplitudes of each component of the response at time t=0. In some instances, rather than just quote both of the time constants and their respective initial amplitudes, a single 'weighed' decay constant is reported. Some times this is because a comparison is being made between different synapses that may or may not have single exponential decays. To calculate the 'weighted' mean time constant, the individual initial amplitudes for each time constant are expressed as a fraction of the total initial amplitude. Lets call these fractions A and B, such that A = a / (a+b) and B = b / (a+b) Lets then call the 'weighted' mean decay constant T, and this is given by: T = A * t1 + B * t2 So you see, you get a indication of the exponential decay by 'weighting' the individual time constants according to the initial amplitude, to get a mean time constant. This is reasonable, given that the initial amplitude and the time constant of each component will determine the proportional contribution to the exponential decay that is being described. I hope this helps. Regards, Trevor From r_s_norman from _comcast.net Thu Jan 15 17:46:38 2009 From: r_s_norman from _comcast.net (r norman) Date: Thu Jan 15 20:02:02 2009 Subject: [Neuroscience] Re: Decay constants. What does "weighted" mean? References: <86e1f737-b55f-4a73-92ee-a59c102d426a@y1g2000pra.googlegroups.com> <0tnum4hfq9q5s3glfjsts7acf15u3rkdnf@4ax.com> Message-ID: On Thu, 15 Jan 2009 18:40:10 +0100, Imre Vida wrote: >On Thu, Jan 15, 2009 at 09:17:00AM -0700, r norman wrote: >> On Thu, 15 Jan 2009 01:01:28 -0800 (PST), Bill >> wrote: >> >> >Hi, >> > >> >Synaptic events decay with an (bi)exponetial function. You can of >> >course report the decay constant, which I understand, but what do >> >people mean when they refer to the weighted decay constant? >> > >> >Thanks. >> >> When a function does not show simple exponential decay, but rather has >> several terms each with a different time constant, then each term has >> a "weight" associated with it >> a exp(-t/t1) + b exp(-t/t2) >> where t1 and t2 are two time constants and a and b are the respective >> "weights". >> >> That is the usual meaning, but describe the use of the term in >> context, or better, the citation with a material and methods sections >> talking about how to calculate the values, and I can describe it >> better. >> >> Note: an RC circuit, of course, has a simple exponential decay but >> synaptic decay is complicated because of the spatial decay >> superimposed on the temporal decay. That is, the partial differential >> equation of the cable equation of the dendritic tree is rather >> different from the simple differential equation of an RC circuit. Of >> course, lingering synaptic activation also can complicate the decay >> pattern. That means that synaptic decay is not simple exponential >> decay. >> > >from this, the weighted decay time constant is: > tw = (a*t1+b*t2)/(a+b) >it is a simplification, to describe the "speed" of >the decay with a single value and enable the comparison >of "events" with different decay kinetics > >i guess when you say synaptic events, you mean E/IPSCs >i.e. currents. Their decay kinetics is dependent on when the >channels close, deactivate or desensitize. Yes, I didn't combine the separate decays into a single "weighted" value. If the synaptic events are, indeed, the currents then the various decay kinetics do relate to the kinetics of decay of the channel closing. I was assuming potentials, in which case the membrane cable properties are the most important aspect, something that will ordinarily completely obscure the channel kinetics. So it really becomes important to see what the original authors are talking about. From jeedward from yahoo.com Fri Jan 16 11:14:38 2009 From: jeedward from yahoo.com (John Edward) Date: Fri Jan 16 12:21:46 2009 Subject: [Neuroscience] Final call for papers: special session on Neuro Science Message-ID: <714295.64484.qm@web45911.mail.sp1.yahoo.com> Special session on Neuro Science at AIPR-09: final call for papers ? There is a special session on?Neuro Science at the 2009 International Conference on Artificial Intelligence and Pattern Recognition (AIPR-09) (website: http://www.PromoteResearch.org) that will be held during July 13-16 2009 in Orlando, FL, USA. We invite draft paper submissions. The conference will take place at the same time and venue where several other international conferences are taking place. The other conferences include: ????????? International Conference on Automation, Robotics and Control Systems (ARCS-09) ????????? International Conference on Bioinformatics, Computational Biology, Genomics and Chemoinformatics (BCBGC-09) ????????? International Conference on Enterprise Information Systems and Web Technologies (EISWT-09) ????????? International Conference on High Performance Computing, Networking and Communication Systems (HPCNCS-09) ????????? International Conference on Information Security and Privacy (ISP-09) ????????? International Conference on Recent Advances in Information Technology and Applications (RAITA-09) ????????? International Conference on Software Engineering Theory and Practice (SETP-09) ????????? International Conference on Theory and Applications of Computational Science (TACS-09) ????????? International Conference on Theoretical and Mathematical Foundations of Computer Science (TMFCS-09) ? The website http://www.PromoteResearch.org contains more details. ? Sincerely John Edward Publicity committee ? ? From connelly.bill from gmail.com Sat Jan 17 23:02:19 2009 From: connelly.bill from gmail.com (Bill) Date: Sun Jan 18 15:31:45 2009 Subject: [Neuroscience] Re: Decay constants. What does "weighted" mean? References: Message-ID: <9247173e-1e8a-42e5-b05e-cd8d89ccd12a@r10g2000prf.googlegroups.com> Thanks Trevor, that explains it nicely (I geussed it was something like that). Why do people do it in that way? Wouldn't it make more sense if you were comparing an intervention to do a 2-way ANOVA with Intervention vs Slow Decay Constant vs Fast Decay Constant? On Jan 16, 11:46?am, Trevor Lewis wrote: > Dear Bill, > > A little more information to add to what r norman posted: > As explained, for a response that can be fitted with the sum of two > exponentials - > ? f(t) = a exp(-t/t1) + b exp(-t/t2) > > where t1 and t2 are the time constants and a and b are the initial > amplitudes of each component of the response at time t=0. > > In some instances, rather than just quote both of the time constants > and their respective initial amplitudes, a single 'weighed' decay > constant is reported. Some times this is because a comparison is > being made between different synapses that may or may not have single > exponential decays. > > To calculate the 'weighted' mean time constant, the individual > initial amplitudes for each time constant are expressed as a fraction > of the total initial amplitude. Lets call these fractions A and B, > such that A = a / (a+b) ?and B = b / (a+b) > Lets then call the 'weighted' mean decay constant T, and this is given by: > T = A * t1 + B * t2 > > So you see, you get a indication of the exponential decay by > 'weighting' the individual time constants according to the initial > amplitude, to get a mean time constant. This is reasonable, given > that the initial amplitude and the time constant of each component > will determine the proportional contribution to the exponential decay > that is being described. > > I hope this helps. > Regards, > > Trevor From t.lewis from unsw.edu.au Mon Jan 19 21:01:23 2009 From: t.lewis from unsw.edu.au (Trevor Lewis) Date: Mon Jan 19 23:29:31 2009 Subject: [Neuroscience] Re: Decay constants. What does "weighted' mean? In-Reply-To: <200901191704.n0JH4x820125@net.bio.net> References: <200901191704.n0JH4x820125@net.bio.net> Message-ID: <7ha0n3$5fp1a@INFPACM003.services.comms.unsw.edu.au> Hi Bill, Why do people do it this way? Let me provide an example that I am most familiar with. Take the development of inhibitory synapses in the lateral superior olive: they start out predominantly comprised of GABA type A receptors and gradually glycine receptors are introduced so that there is a mixture of the two at the synapse and then eventually become predominantly comprised of glycine receptors. The IPSCs from GABAaRs is slow, while GlyRs are fast. In this case it is useful to have a weighted mean time constant to describe the exponential decay of the IPSCs over the different developmental stages - since at some stages there will be two exponential components, and other stages just one component. Thus, the change from the slow IPSCs to the fast IPSCs can be described with a single parameter and can be easily plotted against time. Of course, you wouldn't rely solely on this analysis to describe what is happening. Certainly, if you were wanting to compare the relative contributions of the fast and slow components then a more robust statistical comparison would be useful (like a 2-way ANOVA). Trevor At 04:04 AM 20/01/2009, you wrote: >Date: Sat, 17 Jan 2009 20:02:19 -0800 (PST) >From: Bill >Subject: [Neuroscience] Re: Decay constants. What does "weighted" > mean? >To: neur-sci@net.bio.net >Message-ID: > <9247173e-1e8a-42e5-b05e-cd8d89ccd12a@r10g2000prf.googlegroups.com> >Content-Type: text/plain; charset=ISO-8859-1 > >Thanks Trevor, that explains it nicely (I geussed it was something >like that). > >Why do people do it in that way? Wouldn't it make more sense if you >were comparing an intervention to do a 2-way ANOVA with Intervention >vs Slow Decay Constant vs Fast Decay Constant? From connelly.bill from gmail.com Tue Jan 20 14:54:47 2009 From: connelly.bill from gmail.com (Bill) Date: Tue Jan 20 15:54:11 2009 Subject: [Neuroscience] Re: Decay constants. What does "weighted' mean? References: <200901191704.n0JH4x820125@net.bio.net> Message-ID: <38dc57bd-f4ea-4f79-9095-c84553cae0fc@o4g2000pra.googlegroups.com> Excellent. Again, it makes perfect sense. Thank you very much. On Jan 20, 3:01?pm, Trevor Lewis wrote: > Hi Bill, > > Why do people do it this way? Let me provide an example that I am > most familiar with. Take the development of inhibitory synapses in > the lateral superior olive: they start out predominantly comprised of > GABA type A receptors and gradually glycine receptors are introduced > so that there is a mixture of the two at the synapse and then > eventually become predominantly comprised of glycine receptors. The > IPSCs from GABAaRs is slow, while GlyRs are fast. In this case it is > useful to have a weighted mean time constant to describe the > exponential decay of the IPSCs over the different developmental > stages - since at some stages there will be two exponential > components, and other stages just one component. Thus, the change > from the slow IPSCs to the fast IPSCs can be described with a single > parameter and can be easily plotted against time. Of course, you > wouldn't rely solely on this analysis to describe what is happening. > Certainly, if you were wanting to compare the relative contributions > of the fast and slow components then a more robust statistical > comparison would be useful (like a 2-way ANOVA). > > Trevor > > At 04:04 AM 20/01/2009, you wrote: > > >Date: Sat, 17 Jan 2009 20:02:19 -0800 (PST) > >From: Bill > >Subject: [Neuroscience] Re: Decay constants. What does "weighted" > > ? ? ? ? mean? > >To: neur-...@net.bio.net > >Message-ID: > > ? ? ? ? <9247173e-1e8a-42e5-b05e-cd8d89ccd...@r10g2000prf.googlegroups.com> > >Content-Type: text/plain; charset=ISO-8859-1 > > >Thanks Trevor, that explains it nicely (I geussed it was something > >like that). > > >Why do people do it in that way? Wouldn't it make more sense if you > >were comparing an intervention to do a 2-way ANOVA with Intervention > >vs Slow Decay Constant vs Fast Decay Constant? From davidelan from REMOVECAPITALhotmail.com Mon Jan 26 08:33:15 2009 From: davidelan from REMOVECAPITALhotmail.com (davide) Date: Tue Jan 27 12:32:05 2009 Subject: [Neuroscience] [Probably OT]Combine neuroscience and computer science Message-ID: Hello everybody, I explain a bit the strange subject. By the way I am not sure this is the right NG, apologies if it isn't. I have studied computer science for many years and very recently robotics but now for some reasons (I am not going to bore you with them) I have realised that it is not what I really want to do. Now I am very interested in spirituality (humans and not machines) and in particular in consciousness. Neuroscience is directly related to it and also very fascinating. But I am not sure it's what I had in mind (at the moment I am more interested in the spiritual side of consciousness but I have also started to read about neuroscience). Anyway, I did not want to waste many years of computer science and therefore I was looking for a solution to put the two things together. That's why this post. So, is there a way to combine computer science and consciousness? I know this may sound a bit strange to you but if you have any idea, suggestion, comment, critic ..... I would really appreciate. Many thanks. Davide. From jalegris from sympatico.ca Tue Jan 27 00:14:21 2009 From: jalegris from sympatico.ca (J.A.Legris) Date: Tue Jan 27 12:32:13 2009 Subject: [Neuroscience] Re: Combine neuroscience and computer science References: Message-ID: <1b2c6a07-43f0-46a2-ac54-9a274cdd6259@t26g2000prh.googlegroups.com> On Jan 26, 8:33?am, davide wrote: > Hello everybody, > > I explain a bit the strange subject. By the way I am not sure this is > the right NG, apologies if it isn't. > > I have studied computer science for many years and very recently > robotics but now for some reasons (I am not going to bore you with them) > I have realised that it is not what I really want to do. Now I am very > interested in spirituality (humans and not machines) and in particular > in consciousness. Neuroscience is directly related to it and also very > fascinating. But I am not sure it's what I had in mind (at the moment I > am more interested in the spiritual side of consciousness but I have > also started to read about neuroscience). Anyway, I did not want to > waste many years of computer science and therefore I was looking for a > solution to put the two things together. That's why this post. > So, is there a way to combine computer science and consciousness? > > I know this may sound a bit strange to you but if you have any idea, > suggestion, comment, critic ..... I would really appreciate. > > Many thanks. > > Davide. You may have a point there, lumping consciousness in with spirituality, because for the most part people who think they are studying consciousness are actually just playing word games. Neuroscience is something completely different - it is biology, with no connections to computer science beyond those we find in other fields of science. -- Joe From jalegris from sympatico.ca Wed Jan 28 00:00:57 2009 From: jalegris from sympatico.ca (J.A.Legris) Date: Wed Jan 28 09:31:33 2009 Subject: [Neuroscience] Re: Combine neuroscience and computer science References: <1b2c6a07-43f0-46a2-ac54-9a274cdd6259@t26g2000prh.googlegroups.com> <5IIfl.42433$1L3.11834@newsfe20.iad> Message-ID: <08f2b9b4-33ed-423f-b8e9-d43a351183e0@v42g2000yqv.googlegroups.com> On Jan 27, 1:49?pm, "paradox137" wrote: > You may have a point there, lumping consciousness in with > spirituality, because for the most part people who think they are > studying consciousness are actually just playing word games. > > What about the report that 50 hertz sound that one would hear in from a > church organ > makes you feel as if you were with God. > > Ron Blue Evidently God resonates at a fairly snappy 50 Hertz, much higher than I would have predicted. -- Joe From divyarathore from gmail.com Wed Jan 28 03:24:04 2009 From: divyarathore from gmail.com (divya_rathore_@gmail.com) Date: Wed Jan 28 09:31:43 2009 Subject: [Neuroscience] Re: Combine neuroscience and computer science References: Message-ID: On Jan 26, 6:33?pm, davide wrote: > Hello everybody, > > I explain a bit the strange subject. By the way I am not sure this is > the right NG, apologies if it isn't. > > I have studied computer science for many years and very recently > robotics but now for some reasons (I am not going to bore you with them) > I have realised that it is not what I really want to do. Now I am very > interested in spirituality (humans and not machines) and in particular > in consciousness. Neuroscience is directly related to it and also very > fascinating. But I am not sure it's what I had in mind (at the moment I > am more interested in the spiritual side of consciousness but I have > also started to read about neuroscience). Anyway, I did not want to > waste many years of computer science and therefore I was looking for a > solution to put the two things together. That's why this post. > So, is there a way to combine computer science and consciousness? > > I know this may sound a bit strange to you but if you have any idea, > suggestion, comment, critic ..... I would really appreciate. > > Many thanks. > > Davide. Directly or indirectly, Diffusion Tensor Imaging (DTI) and fMRI (functional MRI) are contributing towards what you are asking for. - Divya Rathore www.adislindia.com/people/~divya/index.htm From kldickson from wisc.edu Wed Jan 28 07:22:56 2009 From: kldickson from wisc.edu (KATHARINE LEAH DICKSON) Date: Wed Jan 28 09:31:51 2009 Subject: [Neuroscience] Re: Combine neuroscience and computer science In-Reply-To: <1b2c6a07-43f0-46a2-ac54-9a274cdd6259@t26g2000prh.googlegroups.com> References: <1b2c6a07-43f0-46a2-ac54-9a274cdd6259@t26g2000prh.googlegroups.com> Message-ID: Studying consciousness in neuroscience, I think, requires a knowledge of what consciousness actually is. It's not impossible to study it - Giulio Tononi at my institution is doing some research related to sleep, and I think Tristan Bekinschtein at Cambridge is doing research on 'disorders of consciousness', but I don't know how you'd approach it from computational paths since much of 'consciousness' is colored by human emotions, which computers cannot simulate. Katharine Leah Dickson kldickson@wisc.edu ----- Original Message ----- From: "J.A.Legris" Date: Tuesday, January 27, 2009 11:35 am Subject: [Neuroscience] Re: Combine neuroscience and computer science To: neur-sci@magpie.bio.indiana.edu > On Jan 26, 8:33?am, davide wrote: > > Hello everybody, > > > > I explain a bit the strange subject. By the way I am not sure this > is > > the right NG, apologies if it isn't. > > > > I have studied computer science for many years and very recently > > robotics but now for some reasons (I am not going to bore you with > them) > > I have realised that it is not what I really want to do. Now I am very > > interested in spirituality (humans and not machines) and in particular > > in consciousness. Neuroscience is directly related to it and also very > > fascinating. But I am not sure it's what I had in mind (at the > moment I > > am more interested in the spiritual side of consciousness but I have > > also started to read about neuroscience). Anyway, I did not want to > > waste many years of computer science and therefore I was looking > for a > > solution to put the two things together. That's why this post. > > So, is there a way to combine computer science and consciousness? > > > > I know this may sound a bit strange to you but if you have any idea, > > suggestion, comment, critic ..... I would really appreciate. > > > > Many thanks. > > > > Davide. > > You may have a point there, lumping consciousness in with > spirituality, because for the most part people who think they are > studying consciousness are actually just playing word games. > Neuroscience is something completely different - it is biology, with > no connections to computer science beyond those we find in other > fields of science. > > -- > Joe > _______________________________________________ > Neur-sci mailing list > Neur-sci@net.bio.net > http://www.bio.net/biomail/listinfo/neur-sci > From jalegris from sympatico.ca Wed Jan 28 10:36:57 2009 From: jalegris from sympatico.ca (J.A.Legris) Date: Wed Jan 28 12:36:44 2009 Subject: [Neuroscience] Re: Combine neuroscience and computer science References: <1b2c6a07-43f0-46a2-ac54-9a274cdd6259@t26g2000prh.googlegroups.com> Message-ID: On Jan 28, 7:22?am, KATHARINE LEAH DICKSON wrote: > Studying consciousness in neuroscience, I think, requires a knowledge of what consciousness actually is. ?It's not impossible to study it - Giulio Tononi at my institution is doing some research related to sleep, and I think Tristan Bekinschtein at Cambridge is doing research on 'disorders of consciousness', but I don't know how you'd approach it from computational paths since much of 'consciousness' is colored by human emotions, which computers cannot simulate. > > Katharine Leah Dickson > kldick...@wisc.edu > > ----- Original Message ----- > From: "J.A.Legris" > Date: Tuesday, January 27, 2009 11:35 am > Subject: [Neuroscience] Re: Combine neuroscience and computer science > To: neur-...@magpie.bio.indiana.edu > > > On Jan 26, 8:33?am, davide wrote: > > ?> Hello everybody, > > > ?> I explain a bit the strange subject. By the way I am not sure this > > is > > ?> the right NG, apologies if it isn't. > > > ?> I have studied computer science for many years and very recently > > ?> robotics but now for some reasons (I am not going to bore you with > > them) > > ?> I have realised that it is not what I really want to do. Now I am very > > ?> interested in spirituality (humans and not machines) and in particular > > ?> in consciousness. Neuroscience is directly related to it and also very > > ?> fascinating. But I am not sure it's what I had in mind (at the > > moment I > > ?> am more interested in the spiritual side of consciousness but I have > > ?> also started to read about neuroscience). Anyway, I did not want to > > ?> waste many years of computer science and therefore I was looking > > for a > > ?> solution to put the two things together. That's why this post. > > ?> So, is there a way to combine computer science and consciousness? > > > ?> I know this may sound a bit strange to you but if you have any idea, > > ?> suggestion, comment, critic ..... I would really appreciate. > > > ?> Many thanks. > > > ?> Davide. > > > ?You may have a point there, lumping consciousness in with > > ?spirituality, because for the most part people who think they are > > ?studying consciousness are actually just playing word games. > > ?Neuroscience is something completely different - it is biology, with > > ?no connections to computer science beyond those we find in other > > ?fields of science. > > > ?-- > > ?Joe Thanks for mentioning Tonini, you reminded me of a fine book. It's a good example of a scientific approach to the subject where computation is seen as a tool rather than a substrate: Gerald Edelman and Giulio Tononi (2001). A Universe Of Consciousness: How Matter Becomes Imagination http://www.amazon.com/Universe-Consciousness-Matter-Becomes-Imagination/dp/0465013775 Here's another I haven't read yet that comes highly recommended: Gyorgy Buzsaki (2006). Rhythms of the Brain http://www.amazon.com/Rhythms-Brain-Gyorgy-Buzsaki/dp/0195301064 Also, if you want to understand consciousness, consider the continuity of brain structure/function across time and phyla. This one I can personally recommend: Georg F. Striedter (2004). Principles of Brain Evolution http://www.amazon.com/Principles-Brain-Evolution-Georg-Striedter/dp/0878938206 -- Joe From Ana.Cervera-Ferri from uv.es Thu Jan 29 09:57:12 2009 From: Ana.Cervera-Ferri from uv.es (Ana.Cervera-Ferri@uv.es) Date: Thu Jan 29 11:52:11 2009 Subject: [Neuroscience] Re: Neur-sci Digest, Vol 44, Issue 12 In-Reply-To: <200901281711.n0SHBf817558@net.bio.net> References: <200901281711.n0SHBf817558@net.bio.net> Message-ID: <1622437895apicerfe@uv.es> Hi all, Perhaps you could have a look at the Christoff Koch lab' web page: http://www.klab.caltech.edu/ > Send Neur-sci mailing list submissions to > neur-sci@net.bio.net > > To subscribe or unsubscribe via the World Wide Web, visit > http://www.bio.net/biomail/listinfo/neur-sci > or, via email, send a message with subject or body 'help' to > neur-sci-request@net.bio.net > > You can reach the person managing the list at > neur-sci-owner@net.bio.net > > When replying, please edit your Subject line so it is more specific > than "Re: Contents of Neur-sci digest..." > > > Today's Topics: > > 1. [Probably OT]Combine neuroscience and computer science (davide) > 2. Re: Combine neuroscience and computer science (J.A.Legris) > 3. Re: Combine neuroscience and computer science > (divya_rathore_@gmail.com) > 4. Re: Combine neuroscience and computer science (J.A.Legris) > 5. Re: Re: Combine neuroscience and computer science > (KATHARINE LEAH DICKSON) > > > ---------------------------------------------------------------------- > > Message: 1 > Date: Mon, 26 Jan 2009 14:33:15 +0100 > From: davide > Subject: [Neuroscience] [Probably OT]Combine neuroscience and computer > science > To: neur-sci@net.bio.net > Message-ID: > Content-Type: text/plain; charset=ISO-8859-1; format=flowed > > Hello everybody, > > I explain a bit the strange subject. By the way I am not sure this is > the right NG, apologies if it isn't. > > I have studied computer science for many years and very recently > robotics but now for some reasons (I am not going to bore you with them) > I have realised that it is not what I really want to do. Now I am very > interested in spirituality (humans and not machines) and in particular > in consciousness. Neuroscience is directly related to it and also very > fascinating. But I am not sure it's what I had in mind (at the moment I > am more interested in the spiritual side of consciousness but I have > also started to read about neuroscience). Anyway, I did not want to > waste many years of computer science and therefore I was looking for a > solution to put the two things together. That's why this post. > So, is there a way to combine computer science and consciousness? > > I know this may sound a bit strange to you but if you have any idea, > suggestion, comment, critic ..... I would really appreciate. > > Many thanks. > > Davide. > > > ------------------------------ > > Message: 2 > Date: Mon, 26 Jan 2009 21:14:21 -0800 (PST) > From: "J.A.Legris" > Subject: [Neuroscience] Re: Combine neuroscience and computer science > To: neur-sci@net.bio.net > Message-ID: > <1b2c6a07-43f0-46a2-ac54-9a274cdd6259@t26g2000prh.googlegroups.com> > Content-Type: text/plain; charset=ISO-8859-1 > > On Jan 26, 8:33?am, davide wrote: > > Hello everybody, > > > > I explain a bit the strange subject. By the way I am not sure this is > > the right NG, apologies if it isn't. > > > > I have studied computer science for many years and very recently > > robotics but now for some reasons (I am not going to bore you with them) > > I have realised that it is not what I really want to do. Now I am very > > interested in spirituality (humans and not machines) and in particular > > in consciousness. Neuroscience is directly related to it and also very > > fascinating. But I am not sure it's what I had in mind (at the moment I > > am more interested in the spiritual side of consciousness but I have > > also started to read about neuroscience). Anyway, I did not want to > > waste many years of computer science and therefore I was looking for a > > solution to put the two things together. That's why this post. > > So, is there a way to combine computer science and consciousness? > > > > I know this may sound a bit strange to you but if you have any idea, > > suggestion, comment, critic ..... I would really appreciate. > > > > Many thanks. > > > > Davide. > > You may have a point there, lumping consciousness in with > spirituality, because for the most part people who think they are > studying consciousness are actually just playing word games. > Neuroscience is something completely different - it is biology, with > no connections to computer science beyond those we find in other > fields of science. > > -- > Joe > > > ------------------------------ > > Message: 3 > Date: Wed, 28 Jan 2009 00:24:04 -0800 (PST) > From: "divya_rathore_@gmail.com" > Subject: [Neuroscience] Re: Combine neuroscience and computer science > To: neur-sci@net.bio.net > Message-ID: > > Content-Type: text/plain; charset=ISO-8859-1 > > On Jan 26, 6:33?pm, davide wrote: > > Hello everybody, > > > > I explain a bit the strange subject. By the way I am not sure this is > > the right NG, apologies if it isn't. > > > > I have studied computer science for many years and very recently > > robotics but now for some reasons (I am not going to bore you with them) > > I have realised that it is not what I really want to do. Now I am very > > interested in spirituality (humans and not machines) and in particular > > in consciousness. Neuroscience is directly related to it and also very > > fascinating. But I am not sure it's what I had in mind (at the moment I > > am more interested in the spiritual side of consciousness but I have > > also started to read about neuroscience). Anyway, I did not want to > > waste many years of computer science and therefore I was looking for a > > solution to put the two things together. That's why this post. > > So, is there a way to combine computer science and consciousness? > > > > I know this may sound a bit strange to you but if you have any idea, > > suggestion, comment, critic ..... I would really appreciate. > > > > Many thanks. > > > > Davide. > > Directly or indirectly, Diffusion Tensor Imaging (DTI) and fMRI > (functional MRI) are contributing towards what you are asking for. > > - Divya Rathore > www.adislindia.com/people/~divya/index.htm > > > ------------------------------ > > Message: 4 > Date: Tue, 27 Jan 2009 21:00:57 -0800 (PST) > From: "J.A.Legris" > Subject: [Neuroscience] Re: Combine neuroscience and computer science > To: neur-sci@net.bio.net > Message-ID: > <08f2b9b4-33ed-423f-b8e9-d43a351183e0@v42g2000yqv.googlegroups.com> > Content-Type: text/plain; charset=ISO-8859-1 > > On Jan 27, 1:49?pm, "paradox137" wrote: > > You may have a point there, lumping consciousness in with > > spirituality, because for the most part people who think they are > > studying consciousness are actually just playing word games. > > > > What about the report that 50 hertz sound that one would hear in from a > > church organ > > makes you feel as if you were with God. > > > > Ron Blue > > Evidently God resonates at a fairly snappy 50 Hertz, much higher than > I would have predicted. > > -- > Joe > > > > ------------------------------ > > Message: 5 > Date: Wed, 28 Jan 2009 06:22:56 -0600 > From: KATHARINE LEAH DICKSON > Subject: Re: [Neuroscience] Re: Combine neuroscience and computer > science > To: neur-sci@magpie.bio.indiana.edu > Message-ID: > Content-Type: text/plain; charset=iso-8859-1 > > Studying consciousness in neuroscience, I think, requires a knowledge of what consciousness actually is. It's not impossible to study it - Giulio Tononi at my institution is doing some research related to sleep, and I think Tristan Bekinschtein at Cambridge is doing research on 'disorders of consciousness', but I don't know how you'd approach it from computational paths since much of 'consciousness' is colored by human emotions, which computers cannot simulate. > > Katharine Leah Dickson > kldickson@wisc.edu > > ----- Original Message ----- > From: "J.A.Legris" > Date: Tuesday, January 27, 2009 11:35 am > Subject: [Neuroscience] Re: Combine neuroscience and computer science > To: neur-sci@magpie.bio.indiana.edu > > > > On Jan 26, 8:33?am, davide wrote: > > > Hello everybody, > > > > > > I explain a bit the strange subject. By the way I am not sure this > > is > > > the right NG, apologies if it isn't. > > > > > > I have studied computer science for many years and very recently > > > robotics but now for some reasons (I am not going to bore you with > > them) > > > I have realised that it is not what I really want to do. Now I am very > > > interested in spirituality (humans and not machines) and in particular > > > in consciousness. Neuroscience is directly related to it and also very > > > fascinating. But I am not sure it's what I had in mind (at the > > moment I > > > am more interested in the spiritual side of consciousness but I have > > > also started to read about neuroscience). Anyway, I did not want to > > > waste many years of computer science and therefore I was looking > > for a > > > solution to put the two things together. That's why this post. > > > So, is there a way to combine computer science and consciousness? > > > > > > I know this may sound a bit strange to you but if you have any idea, > > > suggestion, comment, critic ..... I would really appreciate. > > > > > > Many thanks. > > > > > > Davide. > > > > You may have a point there, lumping consciousness in with > > spirituality, because for the most part people who think they are > > studying consciousness are actually just playing word games. > > Neuroscience is something completely different - it is biology, with > > no connections to computer science beyond those we find in other > > fields of science. > > > > -- > > Joe > > _______________________________________________ > > Neur-sci mailing list > > Neur-sci@net.bio.net > > http://www.bio.net/biomail/listinfo/neur-sci > > > > > > ------------------------------ > > _______________________________________________ > Neur-sci mailing list > Neur-sci@net.bio.net > http://www.bio.net/biomail/listinfo/neur-sci > > End of Neur-sci Digest, Vol 44, Issue 12 > **************************************** > > -- ******************************** Ana Cervera Ferri Dept. Anatomia i Embriologia Humana Fac. Medicina i Odontologia Universitat de Val?ncia Avda. Blasco Iba?ez, 15 46010 Val?ncia - Spain tlf (+34) 963983507; 963983602 (lab); 658159181 ******************************** From afraniocd from gmail.com Sat Jan 31 12:38:09 2009 From: afraniocd from gmail.com (afraniocd@gmail.com) Date: Sat Jan 31 13:40:16 2009 Subject: [Neuroscience] Alzheimer Research Message-ID: <0934ec9a-d07b-462c-8723-57c1eebc9d1b@e25g2000vbe.googlegroups.com> Good Afternoon, Does anyone in this group works with alzheimer research? From johnh from goawayplease.com Sat Jan 31 20:40:14 2009 From: johnh from goawayplease.com (John Hasenkam) Date: Sun Feb 1 00:42:41 2009 Subject: [Neuroscience] Re: Alzheimer Research References: <0934ec9a-d07b-462c-8723-57c1eebc9d1b@e25g2000vbe.googlegroups.com> Message-ID: <24KdnbeBGusDYhnUnZ2dnUVZ8hednZ2d@westnet.com.au> http://www.alzforum.org/ wrote in message news:0934ec9a-d07b-462c-8723-57c1eebc9d1b@e25g2000vbe.googlegroups.com... > Good Afternoon, > Does anyone in this group works with alzheimer research? From Andrey.Kajava from crbm.cnrs.fr Tue Jan 20 05:42:07 2009 From: Andrey.Kajava from crbm.cnrs.fr (Andrey Kajava) Date: Sat Feb 7 17:13:31 2009 Subject: [Neuroscience] (no subject) Message-ID: <4975AA6C.8000802@crbm.cnrs.fr> International Jacques Monod Conference: “Protein folds in infectious and neurodegenerative diseases” Aussois (Savoie), France, 25-29 April 2009. The deadline for applications to attend this conference is February 15th 2009. Please email the application(s) and abstract(s) to Andrey Kajava (andrey.kajava@crbm.cnrs.fr). The conference will be held in Aussois (http://www.caes.cnrs.fr/Vacances/Explorer/Aussois. Registration fee includes board and lodging (385 € for PhD students; 575 € for other participants). More information: http://www.cnrs.fr/sdv/cjm/2009/steven_e.html -- passerelle antivirus du campus CNRS de Montpellier --