Psycho-Babble Medication | about biological treatments | Framed
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Re: more info.

Posted by Adam on November 7, 1999, at 19:39:32

In reply to Re: cont. Prozac after bad reaction WHAT FOR? & misc?, posted by Adam on November 7, 1999, at 15:39:42

My last post was based on an explanation of antidepressant action
that I was given by an old psychiatrist a long time ago. While it may
have some validity, some very quick reading I just did (brought on by
reservations I had, given my relationship with the guy), revealed some
possible oversimlifications or inaccuracies in this explanation of
the delayed onset of antidepressant action in relation to serotonin
levels. Perhaps oversimplifications or inaccuracies are inevitable
given the complexity of the changes in neurons caused by antidepressants.

Presynaptic and postsynaptic neurons may indeed undergo certain specific
"desensitizing" changes in response to the increase of serotonin in the
synapse, at least in certain neurons. Overstimulation of 5-HT1A receptors,
for example, can result in lowered rates of firing of both the presynaptic
and postsynaptic neuron, but this effect may be most important, in relation
to depression, when one considers presynaptic neurons in certain regions of
the brain. In one proposed mechanism, increased levels of serotonin (by SSRI)
in the synapse initially leads to a decrease in serotonin synthesis and
release by the serotonergic neuron, a negative feedback response adapted to
maintain normal serotonin levels in the synapse. Initially, this response
remains unmodified, such that serotonin levels in the synapse aren't increased
enough in the short term to bring about a therapeutic response. Over time,
with continued hyperstimulation, 5-HT1A receptor-mediated signalling is inhibited,
and a portion of the negative-feedback loop thus begins to break down. As
neuron firing and serotonin synthesis return to normal levels, and, because
reuptake of serotonin is simultaneously being inhibited, more serotonin is left
in the synapse, and now we are at "therapeutic levels". It is by inhibiting
this specific negative-feedback that 5-HT1A receptor antagonists (ex: pindolol)
are thought to speed up response to SSRIs: They do quickly what must normally
take time to occur (inhibition of 5-HT1A autoreceptor activity), and thus quickly
increase serotonin levels in combination with an SSRI.

Perhaps delayed antidepressant onset is largely a "presynaptic" phenomenon. I
wonder if "poop-out" is a "postsynaptic" phenomenon.




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