cell death in Korsakoff syndrome

F. Frank LeFever flefever at ix.netcom.com
Wed Dec 2 20:57:27 EST 1998


I've had a special interest in mast cells since hearing Rae Silver
describe them in an entirely new light at the NY Academy of Sciences
about 5 yrs ago, and tend to forget that most people (including many
neuroscientists I've polled at Society for Neuroscience meetings) think
of them precisely the way you described them--histamine, allergic
reactions, etc.

Their phenotype can vary from location to location within the body, but
besides histamine they can produce a wide variety of other substaances,
including many cytokines, and can release them in a graded and
selective fashion--not just the classic massive degranulation and
release of histamine.

Effective signals for activation include cytokines and neural impulses.
 For ex., IL-1 can signal them to decrease PAF release and increase NO
release.

Rae Silver's initial work suggested a role in normal reproductive
behavior in birds, mediating between peripheral factors and the
habenula.  Her work preented at SFN last month showed that thalamic
mast cells had migrated from the circulation.

Although usually near blood vessels, they are on the other side of the
BBB, squarely in the parenchyma.  They migrate and/or multiply in many
pathological conditions, with MS getting the most attention in this
regard--they may be agents of demyelination.

Your point re breakdown in BBB in thiamine deficiency suggests a role
for mast cells, in that they are adjacent to the brain/blood interface
and are thought to have an effect on BBB.

My references are all at work (email at home), but Medline search for
Theoharides should turn up something re "new look" of mast cells...also
Blalock??  And of course, Rae Silver, espec review article--Trends in
Neuroscience?? c. 2 years ago??

F. Frank LeFever, Ph.D.
New York Neuropsychology Group


In <742tvn$5hf$1 at nnrp1.dejanews.com> pelorus at coastalnet.com writes: 
>
>
>>
>> However, I also cited a paper at the recent Society for Neuroscience
>> meeting relating mast cell proliferation in the thalamus, preceding
>> focal lesions in thiamine-deficient rats.  I read this as an
argument
>> for a gradual process, but it occurs to me now that although perhaps
>> contributing to prodromal symptoms they could be activated in the
rapid
>> lesioning processes precipitated by a sudden demannd (e.g. glucose
>> infusion).  What is your thinking on this?
>>
>The mast cell is a histamine-containing element of the immune system,
and I
>could only hazard a guess as to why mast cells should accumulate in
the
>thalamus during advanced thiamin deficiency in rats.
>
>There is a direct correlation between the thiamin content of a cell
and its
>level of metabilic activity.  As I noted before, thiamin's membrane
functions
>are intimately connected to solute transport reactions of a
chemiosmotic
>variety.  Brain vascular tissues maintain a "blood-brain" barrier that
acts to
>keep out of neural networks many compounds that are otherwise present
in blood
>and delivered to organs other than the brain.  Thiamin deficiency is
known to
>cause a breakdown in these barrier functions.  This would allow
molecules that
>do not normally appear in brain tissues to diffuse into the
extracellular
>matrix.  Perhaps in this location these molecules cause a mast cell
mediated
>form of "allergy".  It is just a guess.
>
>Robert D. Brown, MD
>
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