Gamma-burst cortical activity in awake behaving macaques.

Electrophysiological recordings during ketamine anesthesia have revealed a slow alternating pattern of high- and low-frequency activity (a "gamma-burst" pattern) that develops along with the onset of general anesthesia. We examine the role of NMDA receptor antagonism in generating the gamma-burst pattern and the link between gamma-bursts and dissociative anesthesia by comparing the effects of ketamine with those of the highly selective NMDA receptor antagonist CGS 19755 on multi-site intracranial electrophysiology and behavior in rhesus macaques. The data show NMDA antagonism alone drives gamma-burst activity, and that it can do so without causing anesthesia. This supports the expanding consensus that ketamine's anesthetic properties are mediated by mechanisms other than NMDA receptor inhibition.