How do first-generation antipsychotics exert their effects in the brain?

First-generation antipsychotics primarily function by blocking dopamine D2 receptors in the brain, especially within the mesolimbic pathway. This pathway is associated with reward and emotional responses, and overactivity of dopamine transmission in this area is thought to contribute to the positive symptoms of schizophrenia, such as hallucinations and delusions. By antagonizing these D2 receptors, first-generation antipsychotics can reduce these symptoms effectively.

The mechanism of action is crucial because it highlights the role of dopamine dysregulation in psychotic disorders. This understanding forms the foundation for why these medications are used in practice and helps to explain their therapeutic effects.

Other options do not accurately describe the primary mode of action for first-generation antipsychotics. Enhancing serotonin receptors, for instance, aligns more with the mechanism of action of many second-generation antipsychotics. Increasing norepinephrine levels is not a mechanism associated with these agents, as they are more focused on dopamine pathways. Similarly, activating GABA receptors does not relate to the primary action of first-generation antipsychotics, though GABAergic systems do play a role in overall brain function and may be involved in the mechanisms of other psychiatric medications.