Final answer:
Studies of phencyclidine (PCP) and its inhibitory effects on NMDA glutamate receptors have contributed to the glutamatergic hypothesis of schizophrenia, which complements the established dopamine hypothesis of the disorder.
Step-by-step explanation:
On the basis of studies of the properties of phencyclidine (PCP), a glutamatergic hypothesis of schizophrenia has been advanced. This hypothesis suggests that part of the condition's pathology may be due to the dysfunctional signaling of the neurotransmitter glutamate within the brain. PCP, a dissociative drug, acts as an antagonist to the NMDA glutamate receptor, demonstrating that disturbances in glutamate signaling can result in symptoms similar to those seen in schizophrenia. This understanding is part of a broader conversation about the biochemical basis of schizophrenia, which includes other hypotheses like the well-known dopamine hypothesis. The dopamine hypothesis has been influential in the treatment of schizophrenia with antipsychotic medications that primarily block dopamine receptors to reduce excessive dopaminergic transmission. However, the glutamatergic hypothesis offers an additional or alternative explanation contributing to the complexity of the condition, as glutamate is the brain's most abundant excitatory neurotransmitter and is key for normal cognitive functions.