antipsychotic

In conditions like schizophrenia, certain brain pathways behave as if their dopamine signal is turned up too loud, producing hallucinations and delusions. An antipsychotic turns that volume down by sitting on dopamine's receptors, so the over-amplified signal is quieted.

The shared mechanism is blockade of the dopamine D2 receptor, a G-protein-coupled receptor. Effective antipsychotic action correlates closely with how well a drug occupies D2 receptors, a relationship that was a landmark clue to the biology of psychosis.

The class divides into 'typical' first-generation agents (such as haloperidol and chlorpromazine), which block D2 strongly, and 'atypical' second-generation agents (such as risperidone, olanzapine, and clozapine), which add blockade of serotonin 5-HT2A receptors and other targets. The atypicals were designed to cause fewer movement side effects, broadening their receptor profile on purpose.

An honest caveat: too much D2 blockade in motor pathways causes Parkinson-like stiffness and other movement disorders, while different agents carry risks such as weight gain or metabolic changes, so antipsychotic choice is a balance of efficacy against a distinctive side-effect profile.