What is the primary mechanism of action (MOA) of Ketamine?

The primary mechanism of action of ketamine is antagonizing NMDA receptors. Ketamine is known as an NMDA receptor antagonist, which means it blocks the action of the neurotransmitter glutamate at these receptors. This action is particularly significant as it disrupts the excitatory neurotransmission that is often associated with pain perception, anxiety, and certain neurodegenerative processes.

Ketamine's NMDA antagonism contributes to its analgesic (pain-relieving) and anesthetic properties, making it a unique agent in emergency medicine and sedation. The resulting dissociative anesthesia achieved through this mechanism allows patients to experience analgesia while remaining in a trance-like state, which is particularly beneficial in settings where traditional sedatives may not be appropriate.

In contrast, agonizing GABA receptors is the mechanism of action for other anesthetics, such as benzodiazepines or barbiturates, and stimulating MOP receptors relates more to opioid action rather than ketamine. Inhibiting the uptake of GABA would potentially lead to increased GABAergic activity, which is not how ketamine functions. Therefore, recognizing the importance of NMDA receptor antagonism is crucial to understanding how ketamine exerts its distinctive effects.