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?
--David Epstein
[email protected]
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