How is the action of Phencyclidine (PCP) believed to be mediated?

The action of Phencyclidine (PCP) is believed to be mediated through the N-Methyl-D-Aspartate (NMDA) receptor-channel complex. PCP is classified as a dissociative anesthetic, and its primary mechanism of action involves antagonism of the NMDA receptor, which is critical for excitatory neurotransmission in the brain. By blocking the NMDA receptor, PCP disrupts the normal functioning of glutamate, a key neurotransmitter involved in cognitive processes, pain perception, and memory. This blockade leads to the characteristic effects of PCP, such as dissociation and alterations in perception.

The NMDA receptors play a significant role in synaptic plasticity and are involved in the pathways that influence learning and memory. When PCP binds to these receptors, it inhibits their activation by glutamate, which can result in cognitive deficits and altered sensory experiences. This action differentiates PCP from substances that primarily impact serotonin, dopamine, or GABA pathways, as the direct influence on the NMDA receptor is central to its pharmacology and the specific effects associated with its use.