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Re: indirect agonists and etc. » psychobot5000

Posted by clipper40 on November 19, 2007, at 22:08:50

In reply to Re: indirect agonists and etc. » clipper40, posted by psychobot5000 on November 19, 2007, at 17:18:59

> > How exactly does the indirect agonist work then? Also, are there only three ways to influence neurotransmitter levels (real or by mimicking) in the brain (agonist, indirect agonist and reuptake inhibitor)?
> >
>
> Well, I'm out of my depth in trying to make an answer, but as I understand it, there are a bunch of ways drugs can act on these neurotransmitter systems - and the nerves they act on. And I believe researchers are still developing different ways for medications to act, too.
>
>
> But, if I'm not wrong, 'indirect agonist' is a term that overlaps with reuptake inhibitors.
> 'Indirect agonist,' as I understand, is a term that applies to medications, which cause more neurotransmitter to be active, thus causing certain nerves to fire more often. So, indirectly, an SSRI 'agonizes' the nerves in serotonin pathways by causing more serotonin to be active in the synapse (the space between the nerve cells where serotonin does its signalling). By being a reuptake inhibitor, it's also an indirect agonist. I suppose some other drugs that increase available neurotransmitters through other actions, like causing more of them to be released, might also be indirect agonists...I'm not sure on that point.
>
> But there are many other ways of going about things. Valium and xanax don't directly agonize a nerve - they just attach to it and cause its receptors to change shape until they're more likely to be activated by other chemicals. Benadryl and other antihistamines are actually 'antagonists,' meaning they attach to the receptor, but don't cause it to fire - they just block it from being activated by anything else - in effect shutting the nerve down.
>
> But another way meds can effect neurotransmitter levels is by attaching to a different type of receptor - an 'autoreceptor,' whose job it is (at least in some areas) to reduce neurotransmitter release if the levels get too high. So the drug activates it, and it reduces levels of neurotransmitter there.
>
> As far as I can tell, it's all terribly complicated - though some of the posters on this site seem to have a pretty thorough understanding of these things. But of course, please take my words with a grain of salt - they're just my own imperfect understanding, and I may have made some errors (I hope not!).
>
> P-bot


I figured that effecting the autoreceptors would be another way to go. Thanks so much for all of that information. I really appreciate you taking the time to spell it all out for me.

C40


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