Sooooo, why could anyone possible want amisulpridefor their anxiety disorder? Because it has many interesting effects and qualities:
1st. It spectacularly rises GHB receptors (upregulates) and also binds to them (activates), which of course will equally rise GHB activity, which, by all acounts IS VERY VERY EUPHORIC (also, this is a fact, and not up to discussion).
2nd.At low doses (50mg~200mg) Amisulpridewill actually cause dopaminergic neurons (nerve cells which predominantly communicate using dopamine as their main neurotransmitter) TO RELEASE MORE DOPAMINE. Why? Because at those doses it binds to the pre-synaptic receptors. Not following? Simplest terms I said: A synapsis is where two neurons reach each other (an axon and a dendrite). The neuron sending the message has a vesicle (basically a bag full of chemicals or neurotransmitters) from where it releases dopamine. But it also has, some distance away, autoreceptors, which are places the dopamine may bind. Why these? Because when the dopamine reaches, and binds to the autoreceptor, it means it's time to stop releasing dopamine from the vesicle. The neuron says: "That's enough, cut the flow." Well, at the doses I pointed, amisulprideblocks those autoreceptors, so dopamine keeps flowing longer, as the neuron can't know how much is enough. Given this fact, Amisulpridecan be a formidable antidepressant, and will likely lift any depression when other meds fail.
3rd.Amisulprideis an atypical antipsychotic, which means, among a few other things, that it causes far less side-effects (extrapyramidal symptoms). Also, they are what we psychiatrists call a "clean drug". That is: when we have a stable an non delusional or hallucinating schizophrenic patient (those are "positive symptoms", whereas a negative symptom would blunted affect) we want to hit the dopamine receptors. But a "dirty drug", like older or typical antipsychotics, would hit several, even unrelated ones. Like chlorpromazine, commercially and popularly known as Thorazine, the very first antipsychotic. That bad boy will antagonize (block) dopamine receptors (D1, D2, D3 and D4), but it will also hit A LOT of other neurotransmitters, to name a few: histaminic (receptors H1 and H2), serotonin (receptors 5-HT1 and 5-HT2), acetylcholine (Muscarinic receptors M1 and M2). Amisulprideonly hits Dopamine (D1 and D2), antagonizing or agonizing depending on what the prescribing doctor wants to achieve. It also hits 5-HT7 (serotonin) receptors with more antidepressant effects. The activation of the GHB receptors will only further increase its antidepressant actions.
Hope I solved many doubts. BTW, I'm a psychiatrist.