Ghost - pre and post synaptic receptors

[iggy131313]

Im addressing this question to ghost but I wanted to put it here so everyone can benefit from it

Ghost I have been thinking about pre and post synaptic receptors......of course what we dont know is that does an antagonist of 5ht1a effect both pre and post synaptic...does st johns wort upregulate pre synaptically as well as post?

well I wanted to present some speculation on my part which might give us some indication

I have wondered for some time at people who have not been on seronergic drugs but antipsychotics who have severe and lasting anhedonia after discontinuation...years after discontinuation..

Now when one looks at this is makes no sense, anhedonia being caused by a severe dopamine inhibition in the PFC...now, using antipsychotics which BLOCK dopamine receptors cause upregulation...so in theory when one stops an antipsychotic one should have MORE receptors in the PFC and indeed the sriatum (tardive dyskinesia etc) than before the treatment, and any anhedonia should stop.

I dont belive dopamine neurons are destroyed, ive seen this happen after very short term use.....

which led me to consider PRE synaptoc receptors, dopamine n.euron autoreceptors are D2 but located somatodentritically.....so my theory of lasting anhedonia after AP use is this.....

the brain acts as we expect, but in the case of people with lasting anhedonia post discotinuation they have had severe upregulation PRE synaptically of these D2 receptors, as they behave the same as post, the only difference being that they are located in a differnet position...

This would lead to less dopamine release to hit those post synaptic receptors as again, pre synaptc activation leads to the negative feedback and the brakes on dopamine release

So what im saying is that an antagonist of 5ht1a, without it being specifically a pre synaptoc antagonist would cause upreg (but its pot luck) both pre and post.

what are your thoughts?