Which intravenous anesthetic agent stimulates NDMA receptors as its mechanism of action?

Ketamine is an intravenous anesthetic agent whose mechanism of action involves the stimulation of NMDA (N-methyl-D-aspartate) receptors. It acts primarily as an NMDA receptor antagonist, but its unique pharmacological profile allows it to exhibit some degree of stimulation in certain contexts, particularly at lower doses or in specific patient populations.

Unlike many other anesthetics, Ketamine induces a distinctive state known as dissociative anesthesia, characterized by profound analgesia and amnesia without a complete loss of consciousness. This effect is particularly useful in emergency medicine and in procedures where traditional anesthetics may have undesirable effects. The stimulation of NMDA receptors is significant because these receptors are involved in pain perception and have a role in the mechanisms of anesthesia and analgesia.

Other intravenous anesthetic agents mentioned do not primarily act through the NMDA receptors. Instead, agents like Etomidate and Propofol primarily influence GABA receptors, while Sodium Thiopental acts on the GABA-A receptor as well but lacks the unique NMDA receptor interaction that Ketamine provides. Understanding these distinct pathways helps clarify why Ketamine is recognized for its unique position among anesthetics, making it the correct choice in this context.