question from sci-fi-writer

John H John at faraway.com.au
Sun Sep 2 08:07:02 EST 2001


Maxwell has given you a good start, I would like to also suggest that in
looking at the Basal Ganglia you do some digging around on 'dopamine'(as a
start only) , a key neuromodulator that is at least implicated in many of
the conditions maxwell mentions below. One current idea kicking around is
that amidst the welter of modulator and transmitters and inhibitors the
'final common pathway' is the D1 receptor activity. I don't know enough to
know, but to give you some idea, there are at least 5 known receptors for
dopamine, let alone for serotonin, glutamate, Gaba ... . It is easy to think
purely in terms of excitatory activity, but inhibitory activity, achieved
through a variety of means even for a Single pyramidal cell, is just as
important. So if you want to understand why the Basal Ganglia is so
important here, you will have to look at the chemistry side.

Otherwise,

Research published earlier this year I believe, genetically modified mice
had increased numbers of glutamate (NMDA) receptors in the frontal(pre?)
cortex and did significantly better on the water maze test.

Good overview article by excellent researcher but in depth. Available free
at PNAS.org. site (Thanks to all the scientists pushing to make their work
more widely available. Helps me no end.).

Article: Regional and cellular fractionation of working memory
Authors: Patricia S. Goldman-Rakic
Journal: PNAS Goldman-Rakic 93 (24): 13473. (711K)
Location:
N\Cognitive
Regional and cellular fractionation of working memory
Date obtained: 11/06/00
Web Page:
Date Read: 20/06/00
Date to Review:
Keywords: pfc, dope, mexm, wmexm
Printed: 20/06/00
No = subject: 0
Notes:
ABSTRACT
 This chapter recounts efforts to dissect the cellular and circuit basis of
a memory system in the primate cortex with the goal of extending the
insights gained from the study of normal brain organization in animal models
to an understanding of human cognition and related memory dis-orders.
Primates and humans have developed an extraordi-nary capacity to process
information ''on line,'' a capacity that is widely considered to underlay
comprehension, thinking, and so-called executive functions. Understanding
the interac-tions between the major cellular constituents of cortical
circuits-pyramidal and nonpyramidal cells-is considered a necessary step in
unraveling the cellular mechanisms sub-serving working memory mechanisms
and, ultimately, cogni-tive processes. Evidence from a variety of sources is
accumu-lating to indicate that dopamine has a major role in regulating the
excitability of the cortical circuitry upon which the working memory
function of prefrontal cortex depends. Here, I describe several direct and
indirect intercellular mecha-nisms for modulating working memory function in
prefrontal cortex based on the localization of dopamine receptors on the
distal dendrites and spines of pyramidal cells and on inter-neurons in the
prefrontal cortex. Interactions between mono-amines and a compromised
cortical circuitry may hold the key to understanding the variety of memory
disorders associated with aging and disease.

I don't like the concept "executive processes" but the following may help:


Article: Recent developments in working memory
Authors: Alan Baddeley
Journal: Current Opinion in Neurobiology 1998, 8:234-238
Notes: Research on the visual and verbal subsystems of working memory has
shown vigorous development, with PET, fMRI and behavioural data all
supporting separate systems, with further fractionation being likely.
Analysis of executive processes is revealing a range of subprocesses,
providing a very fruitful field for the interaction of cognitive psychology,
neuropsychology and functional imaging.


Literary wise.

Can't remember the author's name but wonderful old short story, "Flowers for
Algernon", about a man who is intelligence is massively enhanced etc etc.
Old setting but v. good adaptation to the screen with the movie "Charly"
Cliff Robertson as lead, did a great job in the role.

Finally,

Don't fall for the idea that simply increasing attention and memory will
make a smarter human. More likely create pathology in non-pathological
people. I am inclined to think that human brains are already at their
functional limit. Other primates don't get Alzheimers, but then gene
expression rates in the human brain, relative to other primates, are
extraordinarily high, while our gene expression rates in kidney? and spleen
(memory failure, have study archived somewhere) are similiar. Given the time
of the writing of "Flowers for Algernon", the author seems to have been have
rather prescient about the first attempts to enhance intelligence.Now I just
want to know if the earlier mentioned smart mice end up with Alzheimers ...
.

Good luck with your story,



John.

maxwell <mmmaxwell at hotmail.com> wrote in message
news:9mq7o6$3jrm8$1 at ID-81739.news.dfncis.de...
>
> JoshCahoon <joshcahoon at cs.com> wrote in message
> news:20010831182518.04375.00000596 at mb-bh.news.cs.com...
> > Kevin Hoffman wrote:
> >
> > >I am writing a sci-fi story that involves a hypothetical "procedure"
that
> > >increases concentration and memory by some large factor (say 1000X).
> > >I would be very grateful for any information on:
> > >- what region of the brain controls concentration and memory
> >
> > Bilateral loss of the hippocampus results in profound anterograde
amnesia, ie,
> > inability to acquire information after the lesion is sustained. One
theory is
> > that the hippocampus is required to convert short term memory into long
term
> > memory. Hippocampus patients, however, do show approximately normal
ability to
> > learn skills or procedures--they just don't remember having learned.
> > Writings on patient HM and Korsakoff's syndrome might be helpful for
you.
>
> The above is correct, Josh.
> >
> > Children with ADHD are believed by some to  owe their symptoms to
insufficient
> > activity in the frontal cortex, which is believed to inhibit other
structures
> > that subserve impulsive or reflexive behaviors. That might be why a
stimulant
> > seems to calm them down and enhance their concentration abilities.
>
> This is decidedly an odd view. I suggest you consider the co-morbidities
of ADHD, OCD, and
> Tourette's, and the commonalities of behaviour that are present.
> Then, consider the deficits in sequence learning, and of attention,
present in
> Parkinson's, Huntington's, and supranuclear palsy patients.
> Common to all of the preceding is evidence of involvement of subcortical
structures,
> especially of caudo-putamen, globus pallidus, pars interna and reticulata,
and of
> substantia nigra, i.e.,  basal ganglia complex (BG).
> Consider BG with respect to cognitive switching and task-sequence
generation.
> Yes, there are reciprocal projections betwixt BG and frontal cortex (FC),
but also to all
> other cortical regions, and for that matter, to multiple thalamic and
tectal nuclei, and
> to cerebellum.
> 'Insufficient' activity in FC as you note, though consistent with notions
of FC as
> 'executive' loci, does not adequately explain much about why stims work to
'focus' ADHD
> kids-- though neuronal accomodation (similar to 'paradoxical' quiescence)
in subcortical
> structures *does.*
> Take a look at works of Graybiel, and of Mink, for starters.
> Apologies-in-advance as I'll not be back for awhile here-- however it's
nice to see at
> least someone new to the forum who is not spouting  'grand hypotheses'
from an armchair
> that is well-removed from any clinical or laboratory evidence of actual
CNS activity.
>
> -maxwell
>
> > >- if there are any current, experimental procedures of this nature
> >
> > No, not for normal people. But if you do a websearch for "nootropics",
you'll
> > find thousands of pages selling "smart drugs". There is scant evidence
that
> > these are effective.
>
>







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