<p>Amisulpride binds selectively to the human dopaminergic D2 and D3 receptor subtypes without any affinity for D1, D4 and D5 receptor subtypes. Unlike classical and atypical neuroleptics, amisulpride displays low affinity for serotonin, &alpha;- adrenergic, histamine receptor subtypes, muscarinic receptors and sigma sites. In the rodent, it preferentially blocks post synaptic D2 receptors located in the limbic structures as compared to those in the striatum as indicated by its reversal of d-amphetamineinduced hyperactivity without affecting stereotypies. In addition, it does not induce catalepsy and it does not produce D2 hypersensitivity after repeated treatment.<br />
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Moreover, it preferentially blocks pre-synaptic D2/D3 dopamine receptors, producing dopamine release responsible for its disinhibitory effects. This atypical pharmacological profile may explain amisulpride&rsquo;s antipsychotic effect at higher doses through post-synaptic dopamine receptor blockade located in the limbic areas and its efficacy against negative symptoms, at lower doses, through presynaptic dopamine receptor blockade. In addition, the reduced tendency of amisulpride to produce extrapyramidal side effects may be related to its preferential limbic activity.</p>