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Re: The Final Pathway To The Dopaminergic Pot Of G

Posted by Brainbeard on September 13, 2009, at 10:03:34

In reply to Re: The Final Pathway To The Dopaminergic Pot Of G, posted by metafunj on September 13, 2009, at 9:09:27

> Does prozac do anything at the 5 HT2A receptor?

Yes, as an SSRI, Prozac blindly activates 5HT2A-receptors. That is to say, any SSRI tends to blindly stimulate ALL serotonin receptors including all subtypes. 5HT1A-activation may be one of the leading mechanisms behind the (S)SRI's success as antidepressants. 5HT2A-activation is not good, and is probably one of the main reasons for the SSRI's initial (and perhaps partly prolonged) side-effects of increased anxiety and agitation. I'm not sure what happens after sustained activation - down-regulation of 5HT2A-receptors? If so, long-term agonizing of 5HT2A-receptors may have the same outcome as 5HT2A-antagonism, namely (indirect) inhibition of
5HT2A-receptors putting a brake on dopamine and noradrenaline.

>Have you found that drugs with 5 HT2A antagonism exert a strong dopaminergic effect?
>

Well, I have mixed experiences. Low dose Risperdal (0.5mg), a potent 5HT2A-antagonist, seemed to have some pronounced pro-dopaminergic effects on me.

Low dose Geodon (ziprasidone, 5-60mg) was a bit of a disappointment since besides whatever good it was doing me, it also made me feel emotionally flat, which was the opposite of what I had hoped for.

I tried to take amitriptyline doses high enough to reach significant 5HT2A-antagonism, but the antihistaminergic sedation was too much for me to swallow.

Just 25mg of nortriptyline (amitriptyline's metabolite) did help my sleep a lot, combined with Luvox (fluvoxamine) and clomipramine, but I'm not sure if that was due to its mild 5HT2A-antagonism. It might well be. Could also be the NRI though.


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poster:Brainbeard thread:904542
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