Posted by Elizabeth on February 7, 2002, at 13:34:50
In reply to Re: Gabitril and benzos, posted by Stephanie S on February 4, 2002, at 15:37:00
First of all, a note to Stephanie: yes, you cleared up my confusion. Thanks!
> Yes... it was the only reuptake inhibitor... but in a couple previous posts there was discussion of some other GABA-based drugs... So I suppose I was actually saying that the mechanism of the reuptake inhibitor as compared to the mechanism of some of the others that were discussed may work better for some and worse for others... :)
It's interesting how that works. It's possible that our different problems are due to disruptions in neurotransmission at different stages; that could explain why, for example, some people need a drug that increases the amount of a neurotransmitter in one way while others need one that increases it another way (e.g., Effexor vs. MAOI).
There are really only a few mechanisms by which these drugs work (that we know of, anyway). The ones that I can think of are:
direct agonists, such as bromocriptine, amantadine, and Mirapex (DA); or the opioid agonists like morphine, methadone, oxycodone, etc.
direct antagonists: antipsychotics (DA, and in some cases 5-HT); naltrexone (opioid); Serzone and Remeron also antagonize some 5-HT receptors; TCAs (NE alpha-1); beta-blockers (NE beta)
autoreceptor agonists: clonidine (NE)
autoreceptor antagonists: Remeron (NE)
reuptake inhibitors: Prozac, etc. (5-HT); Effexor (5-HT, NE, and at high doses DA); tricyclics (NE and in some cases 5-HT)
metabolism inhibitors: MAOIs (MAO metaboilizes 5-HT, NE, DA); GABA-t inhibitors like Sabril
release enhancers: amphetamine (DA and I think NE)
[NE = norepinephrine; 5-HT = serotonin; DA = dopamine]
Of the illegal/recreational drugs, cocaine is a 5-HT, NE, and DA reuptake inhibitor; heroin is an opioid agonist; MDMA and fenfluramine are 5-HT release enhancers. (So they're not really all that different from the medicines we use, in any pharmacological sense.) Nobody's entirely sure how LSD works but it has something to do with serotonin. Marijuana (or its main active ingredient, rather) has its own receptor, the cannabinoid receptor. Nicotine is a cholinergic agonist (it specifically activates the cholinergic receptor subtype that took its name: the nicotinic receptor) and also an MAO-B inhibitor. Alcohol is kind of complicated (as a rule, the simpler the molecule, the more complicated the mechanism -- read up on lithium if you don't believe me :-) ).
-elizabeth
poster:Elizabeth
thread:87498
URL: http://www.dr-bob.org/babble/20020131/msgs/93197.html