Benjamin T Acland, Ben Julian A Palanca, Janine Bijsterbosch, Lawrence H Snyder
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引用次数: 0
Abstract
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 underscores the involvement of mechanisms other than NMDA antagonism in the anesthetic effects of ketamine.
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