Posted by metafunj on September 19, 2009, at 21:06:50
In reply to Re: The Final Pathway To The Dopaminergic Pot Of G, posted by Brainbeard on September 12, 2009, at 6:45:14
Hey Brainbeard I had some questions.
Do you think taking Buspar + Prozac would cause movement disorders in the future due to buspar's D2 antagonism or do you think the increase in DA release from 5 HT2C antagonism would prevent this by increasing dopamine? I'm not sure if this increase is in the same place in the brain that would effect movement.
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?
If SSRIs cause indirect agonism of the 5HT1A receptor how come they don't cause the release of dopamine? 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?The reason I ask about all this meds have caused such a problem in the past that I am fearful of the effects they could have long term. I'm starting to think a stimulant like provigil might be better, but i think it sure would be harder to get a script for.
poster:metafunj
thread:904542
URL: http://www.dr-bob.org/babble/neuro/20090701/msgs/917735.html