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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 4 of 4. This is the beginning of the thread.
Posted by mav27 on September 3, 2008, at 8:57:34
Hi, i have a question about the way amisulpride works. I'll post the info from wiki that explains the part im interested in
" Its dosage ranges from 200 to 1200 mg/day. Lower doses (less than 50 mg) preferentially block D2 autoreceptors that control the synthesis and release of dopamine. This results in an increase in dopaminergic transmission. "
Anyway what i'm wondering is does this only happen at the low dose? When you increase the dose to the typical doses used for psychosis (over 200mg i believe) does the effects of the low dose stop and it just becomes like a typical receptor antagonist or do both actions occur ?
Posted by brot on September 13, 2008, at 11:10:28
In reply to amisulpride, posted by mav27 on September 3, 2008, at 8:57:34
> Hi, i have a question about the way amisulpride works. I'll post the info from wiki that explains the part im interested in
>
> " Its dosage ranges from 200 to 1200 mg/day. Lower doses (less than 50 mg) preferentially block D2 autoreceptors that control the synthesis and release of dopamine. This results in an increase in dopaminergic transmission. "
>
> Anyway what i'm wondering is does this only happen at the low dose? When you increase the dose to the typical doses used for psychosis (over 200mg i believe) does the effects of the low dose stop and it just becomes like a typical receptor antagonist or do both actions occur ?both things occur. more dopamine gets relesed and it gets somewhat blocked at postsynaptic receptors.
brot aka rod
Posted by Brainbeard on September 15, 2008, at 12:27:26
In reply to amisulpride, posted by mav27 on September 3, 2008, at 8:57:34
That's right, except that the D2 blockade is very strong. In fact, even on very small dosages of amisulpride (like 12.5mg), there is enough D2 blockade to make prolactin levels raise sky high.
Posted by bleauberry on September 16, 2008, at 18:12:44
In reply to amisulpride, posted by mav27 on September 3, 2008, at 8:57:34
Like what was already mentioned, both happen at the same time. More dopamine stimulation, but with some blocking of some of that extra dopamine happening downstream.
I know that is hard for us to understand how that could work, but as I've said many times these drugs are way more complicated than the simple neurotransmitter stuff we talk about. They turn certain genes on or off, up or down; they change hormone responses and all the unknown downstream effects of that; there is bleed-through between various neurotransmitter systems; some of that dopamine might be going to receptors that would normally take just serotonin or norepinephrine; some of that dopamine is going to be converted to norepinephrine; the serotonin system is going to respond to that extra dopamine, as well as gaba, glycine, and everything else; we cannot impact one neurotransmitter system without causing changes in the others. Way too complicated for anyone on this planet to understand. We just gotta do the best we can with our primitive basic knowledge and basically let the actual result dictate whether the med is a good thing or not. Theory often doesn't pan out the way it looks on paper.
But yeah, lots of extra dopamine from amisulpride which goes somewhere and does something, but excess amounts of it on the receiving end of the dopamine system are toned down to prevent psychosis.
This is the end of the thread.
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