Yes, amisulpride starts to have antipsychotic effect only in the doses above 200mg or 400mg. I am taking 50mg so it should increase dopamine levels in the synaptic cleft. But in the past I was taking various NDRIs without any positive effect.
I also take very low dose amisulpride, 12.5 mg daily, and find it has a mild mood-boosting effect, as well as helping various ME/CFS symptoms (have a thread about this drug
here).
But when I take the dopamine booster selegiline (deprenyl), I don't get any benefits, even though before getting ME/CFS, I used to use selegiline regularly as a cognitive enhancer, and I found it always had great mood and libido boosting effects, and would increase creativity and lateral thinking abilities as well. But now this same drug does nothing for me (if anything, selegiline now seems to increase my depression slightly).
So that suggests that the dopamine system gets altered as a result of ME/CFS, and does not respond as normal to dopamine drugs.
One study found that 5% of ME/CFS patients have dopamine D2 receptor autoantibodies, so that might in part explain why the dopamine system behaves strangely.
I also tried the NDRI Wellbutrin, and got amazing results for the first two weeks, with my ME/CFS brain fog being greatly improved; but then these very strong positive effects disappeared after two weeks, and thereafter Wellbutrin completely stopped working for me. I've never been able to get it to work ever since. So that's quite odd as well.
But very low dose amisulpride seems to work consistently for me, perhaps because its mechanism of action (working at the dopamine autoreceptors) is an unusual one.
I am quite interested in the dopamine system, because the virus that triggered my ME/CFS (like coxsackievirus B4) also triggered severe anhedonia (the inability to experience reward or pleasure from enjoyable activities), and dopamine plays a key role in the reward circuitry of the brain.
I compiled a list of drugs and supplements that work on the dopamine system
here.