Posted by Brainbeard on February 24, 2010, at 3:42:35
In reply to Re: D2 And 5HT2A: Dopamine Blocking And Boosting » Brainbeard, posted by conundrum on February 23, 2010, at 13:56:46
There does seem to be a huge difference between indirect agonism (SSRI's) and direct antagonism of serotonin subtype receptors (5HT2A/C).
I haven't taken Prozac in normal doses, only low doses, so I can't evaluate the difference between Prozac and the other SSRI's.
For me, the mood-lifting and stimulating effects of low dose Prozac do indeed seem to occur immediately, as long as I don't go higher than 5mg a day.
For me, the noradrenergic boost of 25mg of imipramine can make an immediate difference. Imipramine's metabolite desipramine is a strong NRI, but in Holland it isn't available anymore, while it's also nearly impossible to buy it over the internet without a prescription.
I honestly have no clue as to how rat doses compare to human doses.
I don't have the time to find about about the different Ki values.I have been diagnosed as an obsessive med tweaker too. It can make it harder to get meds prescribed. My current doc, a family doc, is against polypharmacy. I have objected to this that many medications, like the TCA's and the new generations antipsychotics, have manifold pharmacological actions in one pill. He had to agree to that.
Oh, one very important point: Stahl has argued that either 5HT2A or -C-antagonism, or SRI, or 5HT1A-agonism IN THEMSELVES might not have much therapeutic value, but that it's the SYNERGY between these pharmacological mechanisms that makes for the antidepressant efficacy.
poster:Brainbeard
thread:907193
URL: http://www.dr-bob.org/babble/neuro/20100223/msgs/937796.html