To add to what David says below, the journal "Philosophical Transactions
of the Royal Society-B (Biological Sciences) recently had a special issue on
the "serotonin hypothesis" (NOTE: it is important to note that it is a
hypothesis
and not just a description) which can be accessed here:
http://rstb.royalsocietypublishing.org/content/367/1601.toc
There is an introductory article that provides a brief overview of the
research:
Paul R. Albert, Chawki Benkelfat, and Laurent Descarries (September 5,
2012 )
Introduction: The neurobiology of depression-revisiting the serotonin
hypothesis. I.
Cellular and molecular mechanisms Phil. Trans. R. Soc. B, 367, 1601
2378-2381; doi:10.1098/rstb.2012.0190 1471-2970
|Abstract
|The serotonin (5-HT) hypothesis of depression dates from the 1960s. It
|originally postulated that a deficit in brain serotonin, corrected by
antidepressant
|drugs, was the origin of the illness. Nowadays, it is generally accepted
that
|recurring mood disorders are brain diseases resulting from the combination,
|to various degrees, of genetic and other biological as well as
environmental
|factors, evolving through the lifespan. All areas of neuroscience, from
genes
|to behaviour, molecules to mind, and experimental to clinical, are actively
|engaged in attempts at elucidating the pathophysiology of depression and
|the mechanisms underlying the efficacy of antidepressant treatments. This
|first of two special issues of Philosophical Transactions B seeks to
provide
|an overview of current developments in the field, with an emphasis on
cellular
|and molecular mechanisms, and how their unravelling opens new perspectives
|for future research.
There are 10 other articles in this issue that are relevant.
-Mike Palij
New York University
[email protected]
P.S. It would be a mistake to claim that it is a "lack" of serotonin that
is the
problem in depression because the drug tianeptine is a "Selective Serotonin
Reuptake ENHANCER" (SSRE), that is, it increases the amount of serotonin.
For one source, see the Wikipedia entry but a PubMed search may be
warranted:
http://en.wikipedia.org/wiki/Tianeptine
I think it is fairer to say that depression is a dysreguation of the normal
levels of
various neurotransmitters and other neurochemicals.
On Mon, 26 Nov 2012 07:45:12 -0800 , David Epstein wrote:
On Mon, 26 Nov 2012, Michael Britt went:
I recently received a couple questions about the effect of SSRIs on
depression and I'm not quite sure of the answer. Would anyone care
to edify us on these questions?
Do people with depression produce enough serotonin, but it just
isn?t getting absorbed? In other words, it gets released and then
just hangs out in the synapse area? Or do they not produce enough
serotonin to begin with and what doesn?t get absorbed creates a
"deficiency"?
As I understand it, SSRIs prevent serotonin from going back into the
originating neuron and MAOs destroy the serotonin left in the
synapse and that medication stops this destruction from
happening. Both of these are designed to keep the serotonin levels
high. Why not just increase the amount of serotonin in the body say
with 5-HTP supplement? Would more serotonin in the synapse allow
more to be absorbed?
My shortest, easiest answer--forgive me for doing it without giving
cites--is that you can't think in global terms about there being "too
much serotonin" or "too little serotonin." Serotonin is released
along distinct pathways within the brain onto specific target regions,
and it does different things in different regions.
This is partly explained by (and partly just complicated by) the fact
that there are at least 14 different subtypes of receptor for
serotonin. The receptors aren't like the serotonin transporter that
SSRIs block. They don't "absorb" serotonin; they're activated by it,
the way a key on your computer keyboard is activated by your finger
(without absorbing your finger!).
What's more, the different types of receptor can change in number or
sensitivity over the course of minutes, hours, days, weeks, or months.
(The words to look up here and upregulation, downregulation,
sensitization, and desensitization.) Those changes, which happen in
slow and complicated ways in response to SSRIs and other
antidepressants, are probably part of what makes the antidepressants
work.
OK?
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