Posted by King Vultan on March 9, 2004, at 9:35:21
In reply to ssri question, posted by dondon on March 8, 2004, at 22:42:20
> Before ssri's came out, why didn't the drug companies
> design their drugs to inhibit serotonin reuptake
> along with blocking the 5-ht2 and 5-ht3 receptors?
> They knew that nonselective stimulation of these receptors
> caused the unwanted sexual side effects and that
> stimulation of the 5-ht1 receptor was the mechanism
> behind these drugs. I know that Prozac blocks
> 5-ht2c receptor. Also, does a reuptake inhibitor stimulate
> the neurotransmitters receptors? Bupropion is a da reuptake
> inhibitor(also stimulates d1,d2,d3 receptors). Noradrenaline
> reuptake inhibitors would also stimulate central
> noradrenergic receptors.
Actually, Stahl (Essential Psychopharmacology, 2nd Ed., 2000) shows Prozac as a 5HT2C agonist. In answer to your question, before they were introduced, I don't think the pharmaceutical companies realized the extent of the problems that SSRIs were going to cause. They were using imipramine and amitriptyline (which both blockade 5HT2A receptors, along with a bunch of other stuff) as examples of pharmacology to stay away from. In Kramer's Listening to Prozac book, I don't think there is even any mention of sexual side effects from Prozac. I think it took a few years for the psychiatric and pharmaceutical communities to become aware of the various drawbacks to SSRIs, just as the MAO inhibitors were not fully understood when they were first released, either.As far as reuptake inhibitors stimulating receptors, all reuptake inhibitors are indirect agonists at the receptors associated with the neurotransmitter they are blocking reuptake of. Thus, bupropion is an indirect dopamine agonist.
Todd
poster:King Vultan
thread:322277
URL: http://www.dr-bob.org/babble/20040308/msgs/322391.html