Final answer:
NMDA receptor antagonists, such as ketamine and PCP, work by blocking the NMDA receptors to prevent excessive calcium influx, potentially leading to neuronal protection. Drugs targeting specific NMDA receptor subunits, like the NR2B subunit, are being researched to reduce side effects and treat neurological symptoms.
Step-by-step explanation:
The mechanism of action that predominantly involves NMDA receptor antagonism is associated with drugs like ketamine and PCP (phencyclidine). These compounds act as antagonists at the NMDA subtype of glutamate receptors, which are crucial for synaptic transmission and plasticity in the brain. NMDA receptor antagonists, like ketamine, can interfere with the normal action of glutamate by blocking the NMDA receptors, preventing excessive calcium influx that could otherwise lead to excitotoxicity and neuronal damage.
Exploration into the selective targeting of specific NMDA receptor subunits such as the NR2B subunit has been conducted to mitigate the side effects associated with general NMDA receptor antagonists. For example, CP-101,606 (Traxoprodil) is a compound that targets the NR2B subunit and has shown potential for treating Parkinsonian and dyskinetic symptoms in animal studies, although its efficacy in human trials is still under investigation.
The mechanism of action primarily involving NMDA receptor antagonism can be found in certain drugs. NMDA receptors are a type of glutamate receptor that play a role in excitatory neurotransmission in the brain.
One example of a drug that acts as an NMDA receptor antagonist is ketamine. Ketamine is used as an anesthetic, but it can also produce hallucinogenic effects at higher doses. By blocking NMDA receptors, ketamine can alter the neurotransmission and produce its effects.