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Re: Amisulpride - and sulpiride

Posted by undopaminergic on March 19, 2008, at 11:20:57

In reply to Re: Amisulpride, posted by amigan on March 12, 2008, at 21:25:55

> I know that i'm going a little of topic, but i'm taking Sulpride (at low dosage too) because it's a lot cheaper and never felt this dopamine rush effect.
> Has any of you tried Sulpiride? How does it feel in comparision to Amisulpride?
> Do you think that Amisulpride is a more potent "mood brightening" drug or not?

My interpretation of the facts is that the main pharmacological difference between sulpiride (SULP) and amisulpride (AMI) is that the latter is longer-lasting: AMI is typically taken once daily, and SULP up to three times daily. Of course, there may be slight differences in binding affinities for receptors, but the main feature of both is the high degree of selectivity for D2-like dopamine receptors (D2 > D3 >> D4). Unlike the other - "dirty" - anti-psychotics (haloperidol, risperidone, olanzapine, etc.), SULP and AMI do not block dopamine D1-like, adrenergic, serotonergic, histaminergic or cholinergic receptors. The feature (which may be shared with pimozide) that makes them uniquely effective for the treatment of dysthymia and atypical depression is their preferential affinity for presynaptic dopamine autoreceptors, the blockade of which enhances the release of neurotransmitter and results in a (somewhat paradoxical) stimulant effect on dopaminergic neurotransmission - as long as the dose is low enough not to result in extensive blockade of postsynaptic receptors. At higher doses - which may be necessary for the treament of psychosis - many of the side-effects so familiar from dirtier antipsychotics (including sedation, weight gain and motor impairments) tend to emerge.

I've tried both SULP and AMI, but it's only with the former that I've had the opportunity to experience the "dopamine rush" - a stimulant effect that beats methylphenidate (including high doses) by a wide margin in my experience.

As others have noticed, tolerance develops. It's my experience that selegiline helps reverse it, and that after approximately a week of selegiline (10 mg/day p.o.) abstinence from dopamine autoreceptor antagonists, a prominent stimulant response is again possible upon resuming the antagonist. I intend to attempt to verify that assumption in a few days.

Furthermore, when selegiline is used in combination with SULP (and presumably AMI), it potentiates the effect of the latter, and allows a longer period of chronic use before all effect is lost (or at least becomes negligible).

In theory, SULP (and thus probably AMI) potentiates the effects of cocaine (and by extension presumably methylphenidate), but I didn't notice that in practice.

Unlike some others, I haven't noticed a pronounced effect on blunted affect.


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