Posted by Brainbeard on July 31, 2009, at 8:34:31
In reply to Re: any success with dopaminergic meds? » Brainbeard, posted by deprime82 on July 31, 2009, at 8:24:31
> of course wellbutrin is a dopamine reuptake inhibitor.. (also a partial agonist) - when I say dopamine activation then I mean that it's boosting the availability of dopamine between the neurons.
I don't think so. Its dopamine reuptake inhibition is way too weak to account for its stimulating effects. This has been discussed elsewhere on the forum.
> can you tell me then what you mean by the difference between that what the agonists do (mimicking dopamine) and what you mean by activating? do you mean that dopaminergic activation is a stronger release of dopamine or so..? like the stimulants do...?
Well, by dopaminergic activation I think of increasing dopamine concentrations and/or firing. That's what dopaminergic stimulants do. DA-agonists don't increase dopamine or dopamine firing itself, but act on dopamine receptors - fooling the brain, as it were, into thinking there's more dopamine around. According to some, this is the reason that the DA-agonists can actually have anti-dopaminergic side-effects (sedation).
> for me selegiline was indeed causing anxiety and I think it was because of the few amphetamine metabolites.. as for me I have read a few posts, which say that the activating and pushing effect of selegiline is mostly due to the amph-metabolites..Hm, I don't really buy that, but it's a matter of opinion perhaps. Selegiline's main mode of action (catecholamine boosting and MAO-B inhibition) is well enough to increase anxiety. MAO-B inhibition is itself activating, so IMNSHO it is nonsense to say that this effect is due mainly to that tiny amount of wrong-enantiomer (= not very effective) amphetamines.
With the EMSAM-patch, you got selegiline without the amphetamines, and people on Emsam get activated and pushed and anxious just the same.
poster:Brainbeard
thread:909139
URL: http://www.dr-bob.org/babble/20090721/msgs/909423.html