From write_to_eimc from ozemail.com.au Tue Jan 1 22:46:21 2008 From: write_to_eimc from ozemail.com.au (Entertained by my own EIMC) Date: Wed Jan 2 13:04:36 2008 Subject: [Neuroscience] Re: New article/reserach-finding relevant to the Actention Selection Serving System References: <47739d7c$0$6841$5a62ac22@per-qv1-newsreader-01.iinet.net.au> Message-ID: <477b0912$0$25508$5a62ac22@per-qv1-newsreader-01.iinet.net.au> Cheers with whishes for a happy - and lucky - new year for you too, Ken! Peter From write_to_eimc from ozemail.com.au Tue Jan 1 23:11:18 2008 From: write_to_eimc from ozemail.com.au (Entertained by my own EIMC) Date: Wed Jan 2 13:04:41 2008 Subject: [Neuroscience] Re: New article/reserach-finding relevant to the Actention Selection Serving System References: <47739d7c$0$6841$5a62ac22@per-qv1-newsreader-01.iinet.net.au> Message-ID: <477b0eea$0$25527$5a62ac22@per-qv1-newsreader-01.iinet.net.au> The article allows me to remain logically (as well as intuitively) confident that my bet - that I have correctly (or not altogether wrongly or inEPTly) concluded that the basal ganglia contains one of the most central and important "actention module switching stations" (within a sufficiently evolved/brainy neuromuscular animal's Actention Selection Serving System") - is a safe one. It also allow me to keep thinking that I have a philosophically finalized Foremost Overview Of Truth that is well placed. %} "Entertained by my own EIMC" wrote in message news:47739d7c$0$6841$5a62ac22@per-qv1-newsreader-01.iinet.net.au... > The concEPT "actention modules" has yet another scientific indicator. > See http://www.nature.com/neuro/journal/v11/n1/abs/nn2024.html > > The concEPT refers to a modularity that is on the whole of course not > neatly localized. As far as some modules are being simultaneously active > (or environmentally and/or endogenously activated) AND functionally > incompatible, they do as if 'compete' against each other [as if for 'the > prize' of becoming a "paid" actention" (i.e. 'paid' in the neurochemical > 'currency' of neurometabolic resources) or (IOW) for becoming a > transiently "dominant" actention (within the repertoire of a neuromuscular > individual's Actention Selection Serving Systems)] by the functural means > of mutual ("lateral") inhibition, and this whilst the competing modules > are being as if encouraged (or as if 'cheered on') by excitatory sensory > signaling or as if discouraged (or as if 'booed') by inhibitory sensory > signaling prompted by present _and past_ environmental factors or features > of influence. > From jose.guzman from medizin.uni-leipzig.de Mon Jan 7 09:44:12 2008 From: jose.guzman from medizin.uni-leipzig.de (SJM Guzman) Date: Mon Jan 7 10:02:30 2008 Subject: [Neuroscience] EPSP slope Message-ID: <1199713452@jose.guzman.medizin.uni-leipzig.de> Hello All I am trying to calculate the EPSP slope in the 2 ms period from the EPSP onset. This value is known to give a measure of the synaptic strength, because it contains only the monosynaptic component of the EPSP. My question is why is the monosynaptic component related with the synaptic strength (i.e. up/down-regulations of receptors). On the other hand, given the kinetics of the EPSP, wouldn't it be more correct to fit the initial component of the EPSP with a monoexponential function and obtain the exponential coefficient as a mesure of the initial EPSP component? Thank you very much in advance! Bye SJM Guzman Mon, 07 Jan 2008 07:35: 27 +0100 From r_s_norman from _comcast.net Mon Jan 7 11:02:19 2008 From: r_s_norman from _comcast.net (r norman) Date: Mon Jan 7 12:37:53 2008 Subject: [Neuroscience] Re: EPSP slope References: <1199713452@jose.guzman.medizin.uni-leipzig.de> Message-ID: <9oi4o3dspor1sk4hgpuemds778oeicm0hn@4ax.com> On Mon, 07 Jan 2008 15:44:12 +0100, SJM Guzman wrote: >Hello All >I am trying to calculate the EPSP slope in the 2 ms period from the EPSP >onset. This value is known to give a measure of the synaptic strength, >because it contains only the monosynaptic component of the EPSP. > >My question is why is the monosynaptic component related with the synaptic >strength (i.e. up/down-regulations of receptors). > >On the other hand, given the kinetics of the EPSP, wouldn't it be more >correct to fit the initial component of the EPSP with a monoexponential >function and obtain the exponential coefficient as a mesure of the initial >EPSP component? > >Thank you very much in advance! > It has been some time since I did this stuff so there may be newer interpretations. My impression is that the epsp slope gives a better measure of the synaptic strength than the amplitude because it is a more direct measure of synaptic current which is mostly capacitative current, Ic = C dV/dt. That is, in the non-synaptic membrane; the ionic synaptic current completes its loop through the non-synaptic membrane as capacitative current. And synaptic current is a direct measure of the opening of synaptic channels. The notion of connecting this to monosynaptic connections seems strange. A polysynaptic connection through serial synapses would have no effect on the final synaptic step, which is the only one you measure. If you mean parallel synaptic connections, then if more than one synapse fires simultaneously, you would never see it. However if there is a time delay between them then you might be able to see multiple peaks in the current -- that is, in the slope. From a from b.c Tue Jan 8 08:49:53 2008 From: a from b.c (PiottiForEver) Date: Tue Jan 8 12:32:55 2008 Subject: [Neuroscience] Free EEG/ERP resources! Message-ID: <4cLgj.40948$8j3.11627@tornado.fastwebnet.it> Hello to all. For those of you who are interested in EEG/ERP there are free tools available at www.brainterface.com. Luigi From marc.wossner from gmx.net Tue Jan 8 18:46:56 2008 From: marc.wossner from gmx.net (Marc Wossner) Date: Tue Jan 8 23:57:55 2008 Subject: [Neuroscience] What causes the characteristic curve of photoreceptors? Message-ID: <8cf9e650-344a-4338-88f8-fab9dc7a3d9c@l6g2000prm.googlegroups.com> dear ng, can someone help me with the following: What is the characteristic curve of our rod and cone photoreceptors determined by? I found some plots of in vivo measurings of cone receptor potentials that show a clear s-form (http://www.handprint.com/HP/WCL/color4.html#lightadapt, scroll down a bit). That is a kind of toe in the lower part, a linear section in the middle and a kind of shoulder in the upper part. So luminance differences are compressed in the toe and in the shoulder but rendered 1:1 in the middle. Is this caused by a kind of nonlinear response to light alone or do other neurophysiological mechanisms, like lateral inhibition, play a role as well? Many thanks for your input! Marc From gmsizemore2 from yahoo.com Thu Jan 10 12:07:18 2008 From: gmsizemore2 from yahoo.com (Glen M. Sizemore) Date: Thu Jan 10 15:31:50 2008 Subject: [Neuroscience] Re: natural intelligence References: <79768e16-edae-4017-97e9-0b2a2ecb619b@e25g2000prg.googlegroups.com> Message-ID: <478650c5$0$2857$ed362ca5@nr2.newsreader.com> wrote in message news:79768e16-edae-4017-97e9-0b2a2ecb619b@e25g2000prg.googlegroups.com... > On Jan 7, 1:08 pm, J P wrote: > >> What does "is to be seen as a set of motor program generators" mean? >> What programs? Software programs? Who does the programming? >> JP > > Perhaps, I should say that I view the brain as first a set of > generators. Each generator is a group of neurons connected by the > genome to constitute a circuit. A circuit that will, if triggered, > produce a sequenced set of axonal pulses. This set of pulses will, > when it reaches the motor neurons, produce a motor act...lifting an arm, > or kicking a leg. The sequenced pulses I call a motor program. The > genome constructs the neural circuit, a motor program generator. The > motor program generator creates a motor program. The motor program > results in a motor act. > >> You are using again the word program without showing who.what creates >> the program. Are you implying that everything is coming from the >> genome? >> JP > > All life flows from the genome. > > The program is created by a motor program generator. If neuron "A" > emits an axonal pulse that is outward bound, and "A: also synapses on > neuron "B", then "B" will emit a pulse after an interval, say five > milliseconds. This pattern of pulses, A followed by B, is what I call > a sequenced series of pulses. One can think of it as a player piano. > The holes in the roll reach the reading head, and produce sequenced > puffs of air that move down the tubes and produce sequenced movements > of the hammers. We hear music. > >> This seems more like the physical description of a "human computer" >> with programs that have to be "seen" by us. But how are we supposed to >> see them? >> JP > > You should not expect to see them, anymore than you can see the puffs > of air. They are ephemeral. We can think of ways of making them > visible, as computer engineers make a sequence of pulses visible on a > CRT, but I think it best to just think of them abstractly. > > Ray As I have said many, many times, what is wrong with what you say is that it is old and terribly limited. You seem to be saying nothing more than Skinner said when he identified operant behavior as "spontaneous" (i.e., not elicited). Add to that, the early work of Hamburger and others, and it is far from clear that you are talking about anything new. And, indeed, you did not seem to point to the fact that such behavior is not controlled by "external stimuli" - at least not in the way that elicited behavior is controlled by external stimuli (although in the laboratory operants can appear to be like reflexes). What you do not talk about is how CPGs become linked or "blended" together, or how stimuli come to control such responses. Missing from your analysis is how "shaping" (differential reinforcement of successive approximations) can produce responses that, as a whole, would never have been observed without such training. I agree that CPGs are intimately related to operant behavior (this is really what you are saying, whether you know it or not, unless you are saying that all behavior is elicited), but I see nothing new in what you have said (except that the importance of CPGs for operant behavior is not widely recognized but is, in fact, a reasonable conclusion from the work of Skinner and Hamburger). Indeed, as I have said many times, you offer very little by way of explaining much of the data concerning the behavior of animals. Even the "physiology" that you offer is hopelessly naïve (the basal ganglia and cerebellum are intimately involved in such behavior). In closing, you have offered a sort of behavioristic analysis of some phenomena, but such interpretations are now almost 100 years old. You are right, though, to take on the criticisms of idiots like "Alpha" who still want the "mind" to be a cause of behavior. From gmsizemore2 from yahoo.com Thu Jan 10 12:13:16 2008 From: gmsizemore2 from yahoo.com (Glen M. Sizemore) Date: Thu Jan 10 15:31:55 2008 Subject: [Neuroscience] Re: natural intelligence References: <79768e16-edae-4017-97e9-0b2a2ecb619b@e25g2000prg.googlegroups.com> <66492c39-e174-4810-8cfc-4e6c2dc60585@s12g2000prg.googlegroups.com> <4783fb25$0$25980$88260bb3@free.teranews.com> <478511a7$0$26054$88260bb3@free.teranews.com> Message-ID: <4786522b$0$2885$ed362ca5@nr2.newsreader.com> "Alpha" wrote in message news:478511a7$0$26054$88260bb3@free.teranews.com... > > wrote in message > news:b9cce7a3-bb32-4164-9fbe-60a5833698ed@k39g2000hsf.googlegroups.com... >> On Jan 8, 6:27 pm, "Alpha" wrote: >>> wrote in message >> >>> > Soul (spirit, essence, psyche, mind, consciousness, awareness, >>> > intelligence, intellect, mentality, self, individuality, persona, >>> > personality, conscious mental field, self awareness, sentience, >>> > executive function). >>> >>> Those are *certainly * not synonomous! Remove "spirit" and "soul" and >>> you >>> have a group of words that describe processes that have ontological >>> status >>> as they have causal links to lower-level phenomena in the great >>> hierarchy of >>> being, or describe sets of such processes. >> >> I don't wish to argue about words. I merely wish to show how many >> words are used to talk about an (entity, process, whatever). Why so >> many? >> >> I argue that it follows from the discussion between Descartes and the >> Princess Elizabeth as to whether the soul had causal powers. Descartes >> would have it so; the Princess not. The practitioners of AI would have >> no soul, for fear of being trashed as dualists. Nevertheless, when >> speaking of the human brain, they demand an actor. So they invent >> words. >> >> I see nothing in the brain but neurons. > > Do you see anything on page 247 of War and Peace but swirling atoms? or > perhaps cellulose and ink blotches? > >> The circuitry connecting up >> the neurons leads the neurons to effectuate motor acts. That's all >> there is. Just neurons doing their thing. My soul has no causal >> powers. > > But your mind does! And it has causal powers that are not recognizable at > the level of description of neurons or molecules or atoms. Even if the "mind" causes behavior, the analysis is empty until one says why the mind causes the behavior that it does. And if you acknowledge that the mind's choices are a function of its exposure to certain historical environments, then you open the door to explanation of behavior in terms of the environments that produced a mind with the characteristics necessary to choose what it does. And, of course, you ignore the notion that the "mind" is simply a surrogate for the histories that produce behavior. From gmsizemore2 from yahoo.com Thu Jan 10 14:44:54 2008 From: gmsizemore2 from yahoo.com (Glen M. Sizemore) Date: Thu Jan 10 15:32:00 2008 Subject: [Neuroscience] Re: GABA b Antagonists.. References: <9b8hj.220021$U01.1413242@twister1.libero.it> Message-ID: <478675b4$0$2858$ed362ca5@nr2.newsreader.com> "Fabio" wrote in message news:9b8hj.220021$U01.1413242@twister1.libero.it... > Are their able to involve memory and learning? Are there studies about > that? > Thank > Fabio from Italy PubMed, Fabio, PubMed. Often people around here will not respond to questions such as the one you ask; do a little searching and come back with questions. Cordially, Glen From k.m.jasmin from brighton.ac.uk Sat Jan 12 13:43:31 2008 From: k.m.jasmin from brighton.ac.uk (Kyle Jasmin) Date: Sun Jan 13 11:36:58 2008 Subject: [Neuroscience] CFP: 2nd UK Postgrad Conference in Cognitive Linguistics Message-ID: <56B5C9BF-E680-462F-94D7-68BEDEB3895D@brighton.ac.uk> (apologies for cross-postings) CALL FOR PAPERS 2nd UK POSTGRADUATE Conference in COGNITIVE LINGUISTICS University of Brighton, 8th of August, 2008, Brighton, UK Website: www.languageandcognition.net/pgccl Affiliated with the Conference on Language, Communication and Cognition, running the 4th ? 7th of August, 2008. (www.languageandcognition.net for details.) The 2nd UK Postgraduate Conference in Cognitive Linguistics provides a forum for postgraduate students working within Cognitive Linguistics, language and cognition, and related areas of research to share and discuss their individual research, current methodologies and frameworks, and future directions of study. Empirical, theoretical, methodological abstracts relating to the following topics are welcome: - Language and communication - Language and cognition - Metaphor - Grammar and conceptualisation - Knowledge structure - Applied cognitive linguistics - Cognitive semantics - Related areas of research Keynote speakers Dr Ewa D?browska, University of Sheffield, England, Vice President of the UK Cognitive Linguistics Association, Editor of Cognitive Linguistics journal. Prof Vyvyan Evans, University of Brighton, England, President of the UK Cognitive Linguistics Association. Workshop chair Dr Daniel Casasanto, Stanford University, USA. Editor of Language and Cognition, an interdisciplinary journal of language and cognitive science (2009 launch). Submission of abstracts Submissions are solicited for the three parallel sessions and the poster session. - Abstracts should not exceed 500 words?references are excluded from this count. - Abstracts should clearly indicate a presentation title. - Abstracts should be anonymous for purposes of blind review. - Abstracts should be formatted as Word, RTF or PDF documents. - Abstracts should be submitted electronically to UKPGCCL@gmail.com. - Please include the following information in the body of your email: title and name of author(s) affiliation email address for correspondence presentation title 3-5 keywords preference for presentation or poster session. Please state in the subject line of your email that this is an abstract submission, i.e., ?Abstract Submission: Name(s)? ABSTRACT DEADLINE: 2nd of April, 2008 For full details please consult the conference website:http://www.languageandcognition.net/pgccl Organisers The conference is organised by Andrea Morgado De Matos and Kyle Jasmin. Contact The conference email address is UKPGCCL@gmail.com Web details are available at: www.languageandcognition.net/pgccl From teuniz from gmail.com Thu Jan 17 06:16:42 2008 From: teuniz from gmail.com (teuniz@gmail.com) Date: Thu Jan 17 09:59:48 2008 Subject: [Neuroscience] EDFbrowser, a new viewer is now available. Message-ID: <68eee82a-ba90-4104-a364-b466b289584b@n20g2000hsh.googlegroups.com> EDFbrowser, a new free opensource multiplatform viewer. - supported fileformats: EDF, EDF+, BDF, Nihon Kohden* - supports montages - annotations - precise measurements by using crosshairs - zoomfunction by drawing a rectangle with the mouse - shows signals from different files at the same time - built in EDF/EDF+/BDF to ASCII converter - built in Nihon Kohden to EDF+ converter (including annotations) - built in EDF/EDF+/BDF compatibility checker - available for Linux and Windows You can download it here: http://www.teuniz.net/edfbrowser From ben from work Fri Jan 25 05:31:58 2008 From: ben from work (Ben) Date: Fri Jan 25 09:38:26 2008 Subject: [Neuroscience] neuron-neuron proximity and synaptic efficacy Message-ID: <2008012510315816807-ben@work> Does anybody know: If two neurons (presynaptic A and postsynaptic B) are close together, will the synaptic efficacy from A to B be higher than if they were further apart, or does physical location really not matter? TIA, Ben. From Matthew.Kirkcaldie from removethis.utas.andthis.edu.au Fri Jan 25 16:51:53 2008 From: Matthew.Kirkcaldie from removethis.utas.andthis.edu.au (Matthew Kirkcaldie) Date: Fri Jan 25 17:16:54 2008 Subject: [Neuroscience] Re: neuron-neuron proximity and synaptic efficacy References: <2008012510315816807-ben@work> Message-ID: In article <2008012510315816807-ben@work>, Ben wrote: > Does anybody know: If two neurons (presynaptic A and postsynaptic B) > are close together, will the synaptic efficacy from A to B be higher > than if they were further apart, or does physical location really not > matter? > > TIA, > Ben. Depends on the synapse, and the proximity of the synapse to the soma of the postsynaptic cell (as well as the geometry of the dendrite it's on), not how close it is to the presynaptic cell. Case in point: synaptic efficacy of Betz cells in the motor cortex on motor neurons in the caudal spinal cord, a metre away. Cheers, MK. -- Posted via a free Usenet account from http://www.teranews.com From herwin from theworld.com Sat Jan 26 05:32:47 2008 From: herwin from theworld.com (Harry Erwin) Date: Sat Jan 26 13:13:55 2008 Subject: [Neuroscience] Fitzhugh-Nagumo Model Query Message-ID: <1ibbjv1.17xh93br78oy6N%herwin@theworld.com> Where does the cubic term in the Fitzhugh-Nagumo model come from? I know it's necessary to get the van der Pol oscillator, but how do they justify it as a simplification of the Hodgkin-Huxley model? -- Harry Erwin My neuroscience wikiwiki is at From ayazsiddiqi61 from yahoo.com Sat Jan 26 14:03:53 2008 From: ayazsiddiqi61 from yahoo.com (ayaz) Date: Sat Jan 26 18:42:54 2008 Subject: [Neuroscience] Effects of high frequency electromagnetic field (EMF) emitted by mobile phones on the human motor cortex Message-ID: <48af60c7-775c-405d-a851-4bcb2a27d797@c4g2000hsg.googlegroups.com> Effects of high frequency electromagnetic field (EMF) emitted by mobile phones on the human motor cortex Satomi Inomata-Terada, Shingo Okabe, Noritoshi Arai, Ritsuko Hanajima, Yasuo Terao, Toshiaki Frubayashi, Yoshikazu Ugawa * Department of Neurology, Graduate School of Medicine, the University of Tokyo, Tokyo, Japan email: Yoshikazu Ugawa (ugawa-tky@umin.net) *Correspondence to Yoshikazu Ugawa, Department of Neurology, Division of Neuroscience, Graduate School of Medicine, the University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Abstract We investigated whether the pulsed high frequency electromagnetic field (EMF) emitted by a mobile phone has short term effects on the human motor cortex. We measured motor evoked potentials (MEPs) elicited by single pulse transcranial magnetic stimulation (TMS), before and after mobile phone exposure (active and sham) in 10 normal volunteers. Three sites were stimulated (motor cortex (CTX), brainstem (BST) and spinal nerve (Sp)). The short interval intracortical inhibition (SICI) of the motor cortex reflecting GABAergic interneuronal function was also studied by paired pulse TMS method. MEPs to single pulse TMS were also recorded in two patients with multiple sclerosis showing temperature dependent neurological symptoms (hot bath effect). Neither MEPs to single pulse TMS nor the SICI was affected by 30 min of EMF exposure from mobile phones or sham exposure. In two MS patients, mobile phone exposure had no effect on any parameters of MEPs even though conduction block occurred at the corticospinal tracts after taking a bath. As far as available methods are concerned, we did not detect any short-term effects of 30 min mobile phone exposure on the human motor cortical output neurons or interneurons even though we can not exclude the possibility that we failed to detect some mild effects due to a small sample size in the present study. This is the first study of MEPs after electromagnetic exposure from a mobile phone in neurological patients. Bioelectromagnetics From baumgrenze from yahoo.com Fri Jan 25 23:58:26 2008 From: baumgrenze from yahoo.com (baumgrenze) Date: Mon Jan 28 22:19:31 2008 Subject: [Neuroscience] Myelination and Blood Cholesterol Titer Message-ID: I would like to propose the hypothesis that there is sufficient human genetic variation that some individuals require differing blood cholesterol titers to achieve optimal myelination, and that this highly important biological function will trigger a feedback mechanism which will set blood cholesterol at the level required for homeostasis. This suggests to me that medical intervention to adjust blood cholesterol to an 'ideal' level viz-a-viz atherosclerosis, while well intentioned, may trigger neurological problems. Perhaps such intervention should not be suggested before a patient is evaluated with regard to neurosynthesis. At a minimum, all patients being treated for hypercholesterolemia should be forewarned to watch for neurological side effects so that their therapy can be adjusted or terminated before difficult to correct neuopathies ensue. I've not found this hypothesis an easy subject for literature research. Does anyone know if such work has been done or is underway? From JHasenkam from gmail.com Mon Jan 28 19:02:58 2008 From: JHasenkam from gmail.com (JHasenkam@gmail.com) Date: Mon Jan 28 22:19:36 2008 Subject: [Neuroscience] Re: Did I damage my prefrontal cortex? References: Message-ID: On Jan 26, 7:31?am, chadmaester wrote: > On Memorial Day, 2004, I was riding my bicycle down the street, and, > stupidly not wearing a helmet, I hit my forehead on a concrete > sidewalk after not making it around a corner. I was going 5-10 MPH. > The impact broke the skin and left me with about a 3-inch scar down > the middle of my forehead, starting about 1/2 above me hairline (seehttp://chadjohnson.ath.cx/scar.jpgfor a picture). I needed 19 > stitches for that. When I hit the sidewalk I rolled to the right once > or twice, bumping the right side of my head (hard enough to leave a > scar) 1 inch above my ear but toward my face between my ear and my > temple. I believe I had a slight concussion. > > I also have a pretty good bump in the bone of my skull that is about 1 > inch wide and maybe 3 inches high. I am not sure whether this was > there before the incident or not (is this likely to be a result of the > accident?). > > I do know that my behavior has become more aggressive and cynical > since, but I am not sure whether this is a result of my departure from > my Christian beliefs (and cynicism toward them; no, I wish to not talk > about Christianity here). Also, I am a college student, and I have a > hard time getting up in the mornings and getting to classes on time. I > also find that I have had a poor short-term memory (e.g. ADD-like; I > have a hard time staying in context in conversations), and I often > have a hard time focusing at work (I am a computer programmer) and get > distracted very easily by email or people coming up and talking to me. > Furthermore, I have a hard time reading books and staying in context > and not getting distracted (namely daydreaming)--but I do know I had > somewhat poor reading comprehension in middle school. Again, I am not > entirely sure to what extent these behaviors were present before my > accident, but I believe they were present at least to a lesser degree > than they are now. > > So, I am wondering two things: 1) how likely is it that I damaged my > prefrontal cortex (or any other part of my brain); and 2) if I did in > fact damage my brain, how bad does the damage sound? There is a distinct possibility of damage occurring here, particularly if the impact involved a twisting of the head at the time of impact. This type of injury can be very difficult to detect so if a clinician does one imaging and says no damage don't take that as gospel. Your symptoms do suggest some level of damage. It might be self limiting, over time these might recede but ideally you need to find a good neuropsychologist who is familiar with mild brain injury and subtle changes it can induce in behavior. Possibly not just your pfc, the contrapoint might be relevant but also the VTA afferents to the frontals are easily damaged and it can be very difficult to detect these lesions. You need to do the following; Ask people who have known you if they have observed any changes in your behavior. Don't tell them why you are asking, be subtle, no leading questions, and ideally elicit such observations without direct questioning. Have some imaging done but don't take a null finding as conclusive. Some neuropsych tests, particularly those designed to measure pfc function, is a good idea. Find good clinicians who will take your reports seriously. If a clinician says the imaging shows no damage and considers that the end of the matter walk out the door and don't pay the bill. Don't accept recommendations for drug intervention, in your case this is not a good idea. Changes in diet and lifestyle can aid recovery, if you have a positive diagnosis then you should consider seeking advice in changes to maximise brain repair. Remember, a great many people are in the same boat and it is not uncommon for such injuries to go unnoticed. So if you are convinced something has changed you may need to persevere until you find a clinician who has experience in treating such injuries and takes your statements seriously. As you are studying I would consider addressing this problem as a priority. Your symptoms probably won't get worse but therapy might also be able to reduce the symptoms. From JHasenkam from gmail.com Mon Jan 28 19:07:15 2008 From: JHasenkam from gmail.com (JHasenkam@gmail.com) Date: Mon Jan 28 22:19:48 2008 Subject: [Neuroscience] Re: Myelination and Blood Cholesterol Titer References: Message-ID: <0811f969-ad2c-4fb3-81f5-7f7195e0970a@j78g2000hsd.googlegroups.com> On Jan 26, 2:58?pm, baumgrenze wrote: > I would like to propose the hypothesis that there is sufficient human > genetic variation that some individuals require differing blood > cholesterol titers to achieve optimal myelination, and that this > highly important biological function will trigger a feedback mechanism > which will set blood cholesterol at the level required for > homeostasis. > > This suggests to me that medical intervention to adjust blood > cholesterol to an 'ideal' level viz-a-viz atherosclerosis, while well > intentioned, may trigger neurological problems. Perhaps such > intervention should not be suggested before a patient is evaluated > with regard to neurosynthesis. At a minimum, all patients being > treated for hypercholesterolemia should be forewarned to watch for > neurological side effects so that their therapy can be adjusted or > terminated before difficult to correct neuopathies ensue. > > I've not found this hypothesis an easy subject for literature > research. Does anyone know if such work has been done or is underway? Yes, some studies have found that reduced cholesterol can impact on memory and cognition. Ironically this effect is more pronounced in the elderly. It has been stated that myelin is 20% cholesterol. The confounders here are that statins reduce coq10 function which can be rather bad for brains and cholesterol in the brain may be from local production not from the liver. If on a statin a coq10 supplement is a good safeguard. Can't help you with literature searches because this computer does not contain my archives. From sudhee26 from gmail.com Mon Jan 28 23:29:24 2008 From: sudhee26 from gmail.com (Sudheendra Rao N R) Date: Tue Jan 29 00:48:22 2008 Subject: [Neuroscience] Re: Did I damage my prefrontal cortex? In-Reply-To: References: Message-ID: Hi, I bet you dont have clinical expertise. Any neurosurgeon or neurologist would consider damage to prefrontal or frontal lobe while having heard that history. There is a formal way of dealing things like these. First as you mentioned its the imaging stuff..MRI is the best but aided-MRIs like diffusion images etc will be able to pick up mild changes. Also there are other imaging modalities which can shed light upon changes in regional circulation. Its generally not given importance because cognitive retraining if needed would hardly be administered. Also a formal neuropsychological assessment will definitely tell us about prefrontal or frontal pathology. If you depend of docs who inturn depend on imaging to tell you stories..you are surely in a wrong place. You need not tell symptoms..to a good doctor..he will expect them and he will get the answers by asking questions to you..ofcourse not Leading questions. regards, Sudheendra. On Jan 29, 2008 5:32 AM, wrote: > On Jan 26, 7:31 am, chadmaester wrote: > > On Memorial Day, 2004, I was riding my bicycle down the street, and, > > stupidly not wearing a helmet, I hit my forehead on a concrete > > sidewalk after not making it around a corner. I was going 5-10 MPH. > > The impact broke the skin and left me with about a 3-inch scar down > > the middle of my forehead, starting about 1/2 above me hairline > (seehttp://chadjohnson.ath.cx/scar.jpgfor a picture). I needed 19 > > stitches for that. When I hit the sidewalk I rolled to the right once > > or twice, bumping the right side of my head (hard enough to leave a > > scar) 1 inch above my ear but toward my face between my ear and my > > temple. I believe I had a slight concussion. > > > > I also have a pretty good bump in the bone of my skull that is about 1 > > inch wide and maybe 3 inches high. I am not sure whether this was > > there before the incident or not (is this likely to be a result of the > > accident?). > > > > I do know that my behavior has become more aggressive and cynical > > since, but I am not sure whether this is a result of my departure from > > my Christian beliefs (and cynicism toward them; no, I wish to not talk > > about Christianity here). Also, I am a college student, and I have a > > hard time getting up in the mornings and getting to classes on time. I > > also find that I have had a poor short-term memory (e.g. ADD-like; I > > have a hard time staying in context in conversations), and I often > > have a hard time focusing at work (I am a computer programmer) and get > > distracted very easily by email or people coming up and talking to me. > > Furthermore, I have a hard time reading books and staying in context > > and not getting distracted (namely daydreaming)--but I do know I had > > somewhat poor reading comprehension in middle school. Again, I am not > > entirely sure to what extent these behaviors were present before my > > accident, but I believe they were present at least to a lesser degree > > than they are now. > > > > So, I am wondering two things: 1) how likely is it that I damaged my > > prefrontal cortex (or any other part of my brain); and 2) if I did in > > fact damage my brain, how bad does the damage sound? > > There is a distinct possibility of damage occurring here, particularly > if the impact involved a twisting of the head at the time of impact. > This type of injury can be very difficult to detect so if a clinician > does one imaging and says no damage don't take that as gospel. Your > symptoms do suggest some level of damage. It might be self limiting, > over time these might recede but ideally you need to find a good > neuropsychologist who is familiar with mild brain injury and subtle > changes it can induce in behavior. > > Possibly not just your pfc, the contrapoint might be relevant but also > the VTA afferents to the frontals are easily damaged and it can be > very difficult to detect these lesions. > > You need to do the following; > > > Ask people who have known you if they have observed any changes in > your behavior. Don't tell them why you are asking, be subtle, no > leading questions, and ideally elicit such observations without direct > questioning. > Have some imaging done but don't take a null finding as conclusive. > Some neuropsych tests, particularly those designed to measure pfc > function, is a good idea. > Find good clinicians who will take your reports seriously. If a > clinician says the imaging shows no damage and considers that the end > of the matter walk out the door and don't pay the bill. > Don't accept recommendations for drug intervention, in your case this > is not a good idea. > Changes in diet and lifestyle can aid recovery, if you have a positive > diagnosis then you should consider seeking advice in changes to > maximise brain repair. > > Remember, a great many people are in the same boat and it is not > uncommon for such injuries to go unnoticed. So if you are convinced > something has changed you may need to persevere until you find a > clinician who has experience in treating such injuries and takes your > statements seriously. As you are studying I would consider addressing > this problem as a priority. Your symptoms probably won't get worse but > therapy might also be able to reduce the symptoms. > > > _______________________________________________ > Neur-sci mailing list > Neur-sci@net.bio.net > http://www.bio.net/biomail/listinfo/neur-sci > -- Think before agree Think before you nod but STOP thinking and You Are God From tehgabriel from web.de Tue Jan 29 12:22:46 2008 From: tehgabriel from web.de (Tom) Date: Tue Jan 29 20:05:10 2008 Subject: [Neuroscience] Question to FM1-43 staining of synaptic vesicles Message-ID: <340814a1-3895-4d44-a4e7-41543ab05f95@i3g2000hsf.googlegroups.com> Hi! Does anybody have some experience with FM1-43 dyes, especially when used for staining of synaptic vesicles? I am using FM1-43 for staining of synaptic vesicles in primary hippocampal cultures (via 600 APs @ 10 HZ). Subsequently i want to measure synaptic release by applying 2 electric pulses (1st: 40AP followed by 2nd: 600AP) and monitor the resulting fluorescence decrease of synaptic spots. After a first look, my results seemed alright and i found my everything in accordance with the data one can find in literature. But a second look got me thinking. Spots i picked away from synapses (on soma or dendrites) showed a pattern of destaining that was similar to the one of the synapses, even though absolute values were different. But more confusing to me, the ratio of destaining after 40APs / destaining after 600AP, which should be an estimate of the readily releasable pool size was identical in synaptic spots, soma/dendrite spots, and even in background pixels! Does anybody have an idea how to explain this confusing result? Thanks for any ideas! Thomas From Matthew.Kirkcaldie from removethis.utas.andthis.edu.au Mon Jan 28 16:33:15 2008 From: Matthew.Kirkcaldie from removethis.utas.andthis.edu.au (Matthew Kirkcaldie) Date: Wed Jan 30 15:30:24 2008 Subject: [Neuroscience] Re: Did I damage my prefrontal cortex? References: Message-ID: In article , chadmaester wrote: > So, I am wondering two things: 1) how likely is it that I damaged my > prefrontal cortex (or any other part of my brain); and 2) if I did in > fact damage my brain, how bad does the damage sound? It's pretty much impossible to acutely damage the cortex by a physical blow without losing consciousness. Of course the forces experienced by your head were relatively serious compared to a normal bump on the head, but the brain is in a fluid-filled cushioned capsule, suspended by elastic fibres within that fluid. If the blow was strong enough for your cortex to bump into the skull lining it may or may not have been slightly bruised but that would have been assessed at the time you had medical attention, and would most likely recover completely. For a brain injury to cause the personality and behaviour changes you describe, it would require damage to the orbital prefrontal cortex, which rests on top of the eye sockets - that usually involves some kind of trauma to the face where the orbital bones push up into the brain there, which is not the kind of injury you had. Furthermore the fact that you are aware of behaviour changes pretty much guarantees that your frontal cortex is intact - if it were damaged to produce changed behaviour, your ability to comprehend the difference from your previous behaviour would go as well. That's why we feel like the same person for our entire lives, despite quite major changes in the brain's capabilities, particularly frontal cortex functions like social judgement and behavioural regulation. Cheers, MK. -- Posted via a free Usenet account from http://www.teranews.com From neural.stem.cells.EJBio from gmail.com Wed Jan 30 10:05:47 2008 From: neural.stem.cells.EJBio from gmail.com (neural.stem.cells.EJBio@gmail.com) Date: Wed Jan 30 15:30:47 2008 Subject: [Neuroscience] Call for papers on Neural Stem Cells/ Stem Cells Message-ID: Call for papers on Neural Stem Cells! You are now invited to submit Neural stem cell studies being conducted in your own labs. This special issue will be a great chance for peer communication and seeking for national collaborations. Please submit such contributions before March 1. Further, you may contribute short-reviews as well as original articles on topics in but not limitted to following lists: Neural Stem Cells transplantation; Neural Stem Cell differentiation; Adult neurogenesis & neural stem cell niche; History and opinions on Neural Stem Cell research (especially in your own country); New methdology for Neural Stem Cell research; Therapeutical application. Manuscripts could be submitted via WORD (DOC) attachment in email and you will soon acknowledge with a receipt. submission to: nscs@yahoo.cn submission to: neural.stem.cells.ejbio@gmail.com Cheers, Special Issue on Neural Stem Cells eJBio Editoral Broad __________________________________ Electronic Journal of Biology From segundojm from neurohost.org Wed Jan 30 17:51:37 2008 From: segundojm from neurohost.org (SJM Guzman) Date: Wed Jan 30 18:26:49 2008 Subject: [Neuroscience] Filling cells with Lucifer yellow Message-ID: <1201729897@segundojm.neurohost.org> Hello All I am trying to obtain some morphological evidence of my recordings in organotypic slices of the cortex. After some attempts of filling the cells with Lucifer yellow (LY) I experienced some difficulties (mainly a profound pipette clogging). I decided to lower the concentration of LY (from 1 to 0. 1mg/mL but I still have some problems. I cannot get a good seal , and after filling part of the cell, the pipette remains so hardly attached to the cell that the cell is detached when I remove my pipette . Strange enough without LY the recordings are possible , although quite uncomfortable in comparison with the acute slices Apart of using Alexa488 in stead of LY, is there any suggestion out there? thank you very much for your help! SJM Guzman Mon, 28 Jan 2008 23:22:55 +0100 From Vyv.Evans from brighton.ac.uk Thu Jan 31 08:44:08 2008 From: Vyv.Evans from brighton.ac.uk (Vyv.Evans@brighton.ac.uk) Date: Thu Jan 31 09:10:15 2008 Subject: [Neuroscience] New MA Programmes in Language & Cognition References: <96E0A50D3844424DA61CD25A0A93C4BC017EC4C4@EXCHANGE2.university.brighton.ac.uk> <96E0A50D3844424DA61CD25A0A93C4BC017EC4C5@EXCHANGE2.university.brighton.ac.uk> Message-ID: <96E0A50D3844424DA61CD25A0A93C4BC017EC4CA@EXCHANGE2.university.brighton.ac.uk> *********************************NEW MA PROGRAMMES*************************************************** Three new MA programmes in Language & Cognition will commence from September 2008 at the University of Wales, Bangor, UK. These are: --MA in Cognitive Linguistics --MA in Language, Communication and Cognition --MA in Anthropological Linguistics Two of these, the very successful MAs in Cognitive Linguistics, and Language, Communication & Cognition are being transferred from the University of Brighton. Applications are now open. Full details, including how to apply, are available on the web here: http://www.vyvevans.net/CLBangor.htm Alternatively, contact Professor Vyv Evans (vyv.evans@brighton.ac.uk), for details. *********************************NEW MA PROGRAMMES*************************************************** From usenet02 from out-of-phase.de Thu Jan 31 12:05:35 2008 From: usenet02 from out-of-phase.de (Christian Wilms) Date: Thu Jan 31 19:17:15 2008 Subject: [Neuroscience] Re: Filling cells with Lucifer yellow References: <1201729897@segundojm.neurohost.org> Message-ID: <1iblahz.r6ml5tdnl2yN%usenet02@out-of-phase.de> Hey Jose! Long time no read :) What I'm not quite certain about in your question is if you just want to visualize the cell during the recording (for that Alexa 488 would be perfect) or if you are planning on fixing the slices for post processing. In case of the latter, I would recommend using Biocytin. Just add it to your regular recording solution and patch the cells as you normally would. Afterwards, fix the slices in paraformaldehyd. After at least 24 hours, you can easily process the cells using an ABC-detection kit and a streptavidin linked fluorophore. I've previously done this with 200 micron cerebellar slices and it worked beautifully - and quick as well. The whole post processing took just about two hours including mounting. I take it your still in the pharmacology department? Cheers, Christian