Mirtazapine enhanced SER activity - versus SSRI enhanced SER activity?

[JohnBoy2000]

Obviously mirtazapine is blocking alpha 2 receptors - disinhibiting release.

SSRI's are blocking the SER transporter.

Base mechanisms aside - does the increased serotonergic activity via either approach - differ in terms of outcome?


I mean, you'd imagine once synaptic transmitter is raised, post synaptic receptor activation occurs - and that's not really gonna differentiate the means by which the SER molecule is maintained or introduced into the synaptic cleft - is it?


But then you may have varying neuronal projections - which causes the brain areas stimulated by enhanced SER to differ between the two?

As in, mirtazapine blocking alpha 2 receptors in the raphe and locus cerolus, causes disinhibition or release of serotonin, in the cortex - perhaps excluding other brain area's that would in fact be reached via a transporter blocker??


In other words - is it possible that alpha 2 blockers like Mirtazapine might miss certain brain regions than transporter blockers like Zoloft?

 

[JohnBoy2000]

Is this like, such an obvious question it's not actually deserving on an answer??

Or just something that's difficult to shed light on?

 

[sekio]

Alpha adrenergic autoreceptors don't control release of serotonin, AFAICT. They're adrenergic and bind norepinephrine/epinephrine/dopamine preferably.