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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 8 of 8. This is the beginning of the thread.
Posted by falconman on December 14, 2003, at 13:41:06
Hi,
Does any one know at what dose Amisulpride loses its antidepressive properties and inhibits D2+D3 receptors. I'm wondering what the highest dose is that I can take for anxiety/depression. I have started at 50mg and I can't find any info on anyone being treated at a higher dose for these means. I'm a bit weary of going upto 100mg just in case it starts acting as an anti-psychotic.
Thanks
Falcon
Posted by btnd on December 14, 2003, at 14:14:08
In reply to Amisulpride, posted by falconman on December 14, 2003, at 13:41:06
I think the highest is 100 mg.
Posted by rod on December 15, 2003, at 16:10:12
In reply to Amisulpride, posted by falconman on December 14, 2003, at 13:41:06
> Hi,
> Does any one know at what dose Amisulpride loses its antidepressive properties and inhibits D2+D3 receptors. I'm wondering what the highest dose is that I can take for anxiety/depression. I have started at 50mg and I can't find any info on anyone being treated at a higher dose for these means. I'm a bit weary of going upto 100mg just in case it starts acting as an anti-psychotic.
> Thanks
> FalconYes, the studies they made were with 50 and 100mg. But I and my doc think this is because they wanted the side-effects to be as low as possible. In theory, dopaminergic stimulation vs. inhibition is at its maximum at 200mg.
I personally felt a little "simple minded" on 150mg. But you might react different..
good luck
and don't be afraid of going up to 100mg. Just check your prolactine level...rod
Posted by DSCH on December 15, 2003, at 22:06:40
In reply to Amisulpride, posted by falconman on December 14, 2003, at 13:41:06
What do these receptors trip off when they are stimulated?
Is there a dose threshold in the neuropharmacology? I don't understand SLS's notation of (pre > post) for amisulpride in his chart.
Posted by scott-d-o on December 15, 2003, at 23:55:12
In reply to D2 and D3, posted by DSCH on December 15, 2003, at 22:06:40
> What do these receptors trip off when they are stimulated?
Amisulpride is an anti-psychotic med, meaning it doesn't "trip off" anything, it actually does just the opposite. It is a dopamine antagonist which means it sits on the receptors dopamine itself usually binds to and does nothing except block dopamine from attaching to that receptor.
> Is there a dose threshold in the neuropharmacology? I don't understand SLS's notation of (pre > post) for amisulpride in his chart.
I'm assuming this means that it preferentially blocks presynaptic receptors more than postsynaptic. Since the cell uses the presynaptic receptors to gauge how much dopamine is already in the synapse and therefore how much should be released, this has the inverse effect of increasing dopamine release. Amisulpride has this effect at 50 to 200mg, then it supposedly starts to antagonise the postsynaptic receptors just as much as the presynaptic (autoreceptors) thus *decreasing* dopamine release. Hope this helps.
scott
Posted by DSCH on December 16, 2003, at 0:56:24
In reply to Re: D2 and D3 » DSCH, posted by scott-d-o on December 15, 2003, at 23:55:12
> > What do these receptors trip off when they are stimulated?
>
> Amisulpride is an anti-psychotic med, meaning it doesn't "trip off" anything, it actually does just the opposite. It is a dopamine antagonist which means it sits on the receptors dopamine itself usually binds to and does nothing except block dopamine from attaching to that receptor.I meant what do these receptors set into action when they are activated naturally by dopamine.
Thanks for the rest.
Posted by scott-d-o on December 16, 2003, at 6:03:34
In reply to Re: D2 and D3 » scott-d-o, posted by DSCH on December 16, 2003, at 0:56:24
> I meant what do these receptors set into action when they are activated naturally by dopamine.
>
> Thanks for the rest.Ah, I apologize for misreading your question but I'm still not sure I completely understand what it is you are asking. I will do my best but I doubt me or anyone else will be able to answer what I think it is asking conclusively. I don't think we as humans are far enough along in our understanding of the human brain to know the exact physiological effects of agonising specific receptors; it is much too complex (dopamine receptors remain particularly elusive). Probably about the only thing I know specifically about D2 receptors is that agonising them helps reduce Parkinson's disease symptoms; at least for a while. Or perhaps you are asking what is the effect of agonising a receptor in general which is simply that it causes transmission of the nerve impulse to the cell housing the receptor?
So to answer your question the best I can, I would say the effect of stimulating those receptors is the exact benefits you see people claiming they have received from low-dose amisulpride or other dopaminergic meds. It can increase motivation, lower social inhibitions, lower fatigue, decrease anxiety. Of course, all this assumes there is a problem with dopamine transmission to begin with, otherwise it will probably cause nothing but adverse affects and perhaps euphoria.
scott
Posted by scott-d-o on December 16, 2003, at 8:15:14
In reply to Re: D2 and D3, posted by scott-d-o on December 16, 2003, at 6:03:34
One more thing to add to this. The effect of stimulating a dopamine receptor has nothing to do with the *type* but rather what *area* of the brain the receptor is located in. However, some areas contain more of a certain type of dopamine receptor than others. For example, stimulating dopamine receptors in the pleasure center of the brain known as the nucleus accumbens is the source of about every addictive drug's nature. The most euphoric, and thus most addictive, combination of drugs known is a combination of heroin and cocaine known as a speedball. These have been administered to rats and shown to increase dopamine in this area to ungodly numbers. It is also how just about everyone who has died of a drug overdose has gone out; either the cocaine allows them to inject heroin until long after they would be passed out or the heroin works so well as a painkiller they can't even feel it when their heart is about to explode from the cocaine.
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