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Ketamine is a dissociative anesthetic, commonly used for analgesia and anesthesia in a variety of pediatric procedures. It acts as a non-competitive antagonist to block ion channels of the N-methyl-D-aspartate receptors (NMDARs). Our previous study showed that repeated ketamine exposure developed a compensatory increase in NMDAR-mediated currents in neurons of the anterior cingulate cortex (ACC) of neonatal rats, and this increase was largely mediated by the GluN2B subunit-containing receptors, a predominant type of NMDARs during embryonic and early development of the brain. These data provide the molecular evidence to support that immature neurons are highly vulnerable to the development of apoptotic cell death after prolonged ketamine exposure.

journal of pain research

The Increased Channel Activity of N-Methyl-D-Aspartate Receptors at Extrasynaptic Sites in the Anterior Cingulate Cortex of Neonatal Rats Following Prolonged Ketamine Exposure