How does PCP affect neurotransmitter activity?

PCP, or phencyclidine, primarily affects neurotransmitter activity by antagonizing the actions of glutamate, which is the main excitatory neurotransmitter in the brain. Specifically, PCP blocks the NMDA (N-methyl-D-aspartate) receptor, which is a subtype of glutamate receptor. This blockade leads to a decreased excitatory signaling in neural circuits, contributing to the dissociative effects associated with PCP use. By inhibiting glutamate activity, PCP alters cognitive functions, perceptions, and overall neuronal excitability, which is significant in understanding its psychoactive effects.

The other options do not accurately describe the primary action of PCP on neurotransmitter systems. While calcium entry is an important mechanism in various cellular activities, PCP's most notable influence is on glutamate receptors rather than directly increasing calcium entry. Likewise, PCP does not stimulate GABA release or enhance serotonin release as a primary mechanism, although it may have indirect effects on these systems due to its overall impact on brain functionality. Understanding these mechanisms is crucial for comprehending the complexities of substance-induced changes in neurotransmission and their implications for treatment and recovery in substance use disorders.