What is the primary mechanism of action of PCP?

The primary mechanism of action of PCP (phencyclidine) is the antagonism of NMDA glutamate receptors. PCP acts mainly by binding to the phencyclidine site on the NMDA receptor, which is a subtype of glutamate receptor. This action inhibits the normal function of the receptor, resulting in a decrease in excitatory neurotransmission. The NMDA receptor is involved in various central nervous system processes, including learning, memory, and perception of pain. By blocking this receptor, PCP produces a range of effects, including dissociation, hallucinations, and changes in perception.

Understanding the role of NMDA receptors in the brain helps clarify why PCP has such unique psychoactive effects. The disruption in glutamatergic transmission can lead to the distinct dissociative and hallucinogenic experiences associated with the drug.

In contrast, options that involve inhibiting serotonin uptake, increasing dopamine reuptake, or blocking GABA receptors do not accurately reflect PCP's action. These mechanisms are associated with other substances or pharmacological agents that affect different neurotransmitter systems and do not describe PCP's primary effects or unique profile as a dissociative anesthetic.