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Does something in this picture exist for Serotonin?

Yes, except in the case of having too much serotonin it's actually beneficial, SSRIs for instance produce elevated post-synaptic levels of serotonin and then there are downstream neurotrophic effects (release of BDNF etc) that result in depression being suppressed and the growth, rather than death, of new neurons. However extremely high levels of synaptic serotonin result in over-stimulation of neurons and other bad effects, aka "serotonin syndrome". Look on the Wikipedia articles I linked for more info.
 
sekio said:
Yes, except in the case of having too much serotonin it's actually beneficial, SSRIs for instance produce elevated post-synaptic levels of serotonin and then there are downstream neurotrophic effects (release of BDNF etc) that result in depression being suppressed and the growth, rather than death, of new neurons. However extremely high levels of synaptic serotonin result in over-stimulation of neurons and other bad effects, aka "serotonin syndrome". Look on the Wikipedia articles I linked for more info.
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some "SSRIs" seem to increase SERT and decrease synaptic serotonin, at last after a period of weeks. I think they might decrease it during the initial (go postal) 6 weeks or so, acouple of papers speculate a later increase above baseline due to a "hormetic effect" or "rebound".
 
Acute administration of SSRIS will pretty certainly increase post synaptic serotonin, after all SSRIs bind to & block SERT. It's only after the body adapts to this by decreasing release/production of serotonin via stimulation of autoreceptors.

Disclaimer: this is just how I understand it.
 
trainman04 said:
some "SSRIs" seem to increase SERT and decrease synaptic serotonin, at last after a period of weeks. I think they might decrease it during the initial (go postal) 6 weeks or so, acouple of papers speculate a later increase above baseline due to a "hormetic effect" or "rebound".
Click to expand...

Its been noted in rodents that after initial administration SSRIs can cause a decrease in the rate of serotonin cell firing (lets differentiate between cell firing and synaptic 5-HT levels here) in some parts of the brain (cortex), however we cannot say what is happening in any individual human.

The initial decrease in serotonin cell firing is surely due to autoreceptor activation and will be desensitized with time - at which point synaptic levels of 5-HT can really rise and then the brain reaps the beneficial effects

There is a drug that has been used to block serotonin autoreceptors (pindolol) and it has been shown to help augment SSRI response/decrease the time to respond, particularly in the severely depressed patients
 
I've noticed in personal experience that as traditional stims work in a "peak and crash" waveform, specialized SSRI's like Paroxetine and Amoxapine follow an "ebb / rebound" pattern resulting in an overall more balanced neurotransmission state after the initial adjustment period of 2 weeks
 
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