Conventional antipsychotics, such as chlorpromazine, were developed in the 1950s. They work primarily as dopamine antagonists, especially at D2 receptor sites. After dopamine is released by the presynaptic neuron, chlorpromazine blocks dopamine from binding to receptors on the postsynaptic neuron. Initially, dopamine release increases, but over time, production decreases due to depletion. This leads to reduced dopamine activity, especially in the mesolimbic pathway, which is linked to positive symptoms like hallucinations and delusions. Chlorpromazine also blocks other dopamine receptors (D1, D3, D4, D5) and serotonin receptors, though its main effect is on dopamine.