Psycho-Babble Neurotransmitters | advanced medication issues | Framed
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Re: The Final Pathway To The Dopaminergic Pot Of G

Posted by Brainbeard on September 20, 2009, at 4:54:59

In reply to Re: The Final Pathway To The Dopaminergic Pot Of G » Brainbeard, posted by metafunj on September 19, 2009, at 21:06:50

I think movement disorders or other extrapyramidal side-effects (EPS) are unlikely to be caused by Buspar. To date, I haven't heard of any case of Buspar caused EPS. The partial D2-antagonism is probably too weak for that. Especially when you take it at recommended doses, I don't think there will be a problem. In some trials, people have been taking doses of up to 1200mg of Buspar (as an antipsychotic), apparently without trouble.

5HT2C or -A-antagonism in itself can probably not (completely) prevent EPS; it seems that the reason that the atypical antipsychotics are less likely to induce EPS must rather be seen in their weaker adherence to D2-receptors.

> I've read about some people having dark moods on buspar. Do you have any idea why this could be? Do you think it could be from D2 antagonism or too much of a decrease in serotonin transmittion to other receptors?

I think this is probably a temporary effect of the decrease in serotonergic tone that Buspar causes. It seems that some people experience a transient depressive phase while starting Buspar therapy.

> If SSRIs cause indirect agonism of the 5HT1A receptor how come they don't cause the release of dopamine?

Good question. They very well might indirectly cause a release of dopamine, that might on the other hand be countered by their indirect agonism at 5HT2A/C-receptors.

> It is said because SSRIs agonize the
5HT2A/C receptors they inhibit dopamine release, but Buspar taken with an SSRI can increase dopamine in spite of the indirect 5HT2A/C agonism. So if buspar acts just like serotonin, why wouldn't the indirect agonism of an SSRI increase dopamine release and decrease serotonin release similar to Buspar?

Indirect or direct agonism probably makes a big difference. Direct agonism of 5HT2B-receptors, for instance, is likely to cause heart valve damage. The ergoid dopamine-agonists are 5HT2B-agonists and carry this cardiac risk. The indirect 5HT2B-agonism of SSRI's, on the other hand, doesn't seem to cause this cardiovalvulopathy. Also, direct agonism of 5HT2A-receptors is likely to induce hallucinations. Still, the indirect agonism of 5HT2A-receptors by SSRI's is very unlikely to cause hallucinations. So apparently, there is a big difference.

Buspar is really a very mild medication that is practically free of serious side-effects. It can make you a little bit dizzy at medium-high doses (for me: doses above 10mg at a time). Personally, I don't even find this dizziness unpleasant.

If I were you, Buspar would be one of the last meds I would worry about. If it can help you, I would surely take it. It may take some time to reach full therapeutic effect, although in combination with Prozac the dopaminergic boost is immediate.


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poster:Brainbeard thread:904542
URL: http://www.dr-bob.org/babble/neuro/20090701/msgs/917766.html