Posted by psychobot5000 on November 14, 2007, at 22:18:26
In reply to Re: Why aren't stimulants considered dopamine agon » cumulative, posted by clipper40 on November 14, 2007, at 3:49:10
> Thanks. I knew about the functioning of methyphenidate vs. amphetamines. What I didn't understand was the definition of an agonist. I thought an agonist was everything that caused release of neurotransmitter but I see now that it matters if it's directly or indirectly.
Pretty close, yeah. But technically, an 'agonist' doesn't cause release of neurotransmitters - rather, it's like they imitate them in certain places. As I understand it (this isn't likely to be perfect), neurotransmitters have their effects in our nervous systems by attaching to receptors located on nerves. If enough of the molecules attach at a time, then the nerve fires, sending a signal somewhere that has whatever effect. Meds like SSRIs or methylphenidate both are thought to work mainly through 'reuptake inhibition,' meaning that they block the reuptake 'transporter' for a given neurochemical - the thing that's in charge of scooping up excess serotonin, dopamine or whatever for disposal. With it blocked (the transporter), there's more of the chemical to hang around and make the nerves signal. That's how they change things.
Agonists are different. They don't directly change the levels of neurotransmitters. Instead, say, a dopamine agonist, will bind to some of the receptors (usually a post-synaptic receptor) that dopamine normally would, causing those nerves to fire more frequently. Thus, it's directly 'agonising' a nerve in the dopamine system ("dopamine agonist.")
In any case, the end result is usually quite different to just causing extra serotonin or dopamine or whatever to be released. I don't know why that would be entirely, but part of it is probably that a given 'agonist' doesn't necessarily act on all the nerves for a given chemical.
Hope that's helpful!
poster:psychobot5000
thread:794756
URL: http://www.dr-bob.org/babble/20071104/msgs/795175.html