Is it possible receptor activation can differ depending on means of NT enhancement?

[JohnBoy2000]

So - the synaptic neurotransmitter binds to receptor protein, resulting transduction - blah blah.

The means by which the synaptic NT is enhanced - be it via an reuptake blocker - like an SSRI.
Or an autoreceptor, alpha adrenergic blocker - like remeron.

Their bio or physiological "yield", as it were - could the out come differ depending on the means of enhancement?


At the moment - given the contention there is supposedly some cross over of transduction cascades between 5HT and NA, I'm trying to figure out if I can "boost", my noradrenaline combo of mianserin and strattera - with a low dose SSRI.
As Stephen Stahl seems to contend, NRI mechanisms, seem to be more effective with serotonergic enhancement, via SNRI's, versus NRI's in stand alone therapy.

However - I tried a switch back to mirtazapine from mianserin - and it was NOT AN IMPROVEMENT.
It felt like a similar NA boost to mianserin - but something about it gave a horrible sticky unpleasant feeling - which I have to attribute to 5HT enhancement - though I can say that with no form of certainty.


Any opinions?

 

[Cotcha Yankinov]

A key difference between SSRIs and a2 antagonist related 5-HT release is that SERT will have a different spatial expression across the brain/individual cells than a2 expression.

Keep in mind that presynaptic a2 regulate all sorts transmitter release, including acetylcholine release, and acetylcholine receptors in the brain are largely presynaptic, regulating cell firing of lots of other cells. Autoreceptors regulating autoreceptors %)