氯胺酮最显著的电生理作用不足以引起麻醉。

Benjamin T Acland, Ben Julian A Palanca, Janine Bijsterbosch, Lawrence H Snyder
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引用次数: 0

摘要

NMDA受体抑制已被确定为许多精神活性药物、麻醉剂和止痛药的关键功能特性,包括酒精、一氧化二氮、右美沙芬、苯环利定和氯胺酮。本报告通过比较全身注射氯胺酮和高选择性NMDA受体拮抗剂CGS 19755对恒河猴皮层内电生理活动和行为的影响,研究NMDA受体抑制在氯胺酮诱导的麻醉中的作用。亚麻醉剂量的CGS 19755后皮层电生理学的变化类似于麻醉剂量的氯胺酮引起的“伽玛暴”活动,而两种药物的行为效应差异很大。这表明,虽然NMDA拮抗作用足以引起氯胺酮麻醉的关键神经相关性,但其本身不足以引起麻醉。这些发现揭示了以前未被重视的全身NMDA拮抗作用,并阐明了氯胺酮引起的电生理变化与氯胺酮麻醉机制之间的关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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 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. We compare 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. Remarkably, we find that animals given a moderate dose of CGS 19755 are able to perform a difficult memory task, while at the same time showing electrophysiological activity similar to ketamine anesthesia, with one key difference: a lack of delta-band LFP modulation. This difference demonstrates that ketamine's ability to drive strong delta-band oscillations relies on additional mechanisms beyond NMDA receptor antagonism alone, and points to a key role for the activity underlying delta-band oscillations in causing anesthesia.

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