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首页> 美国卫生研究院文献>The Journal of Neuroscience >NMDA Antagonist Ketamine Reduces Task Selectivity in Macaque Dorsolateral Prefrontal Neurons and Impairs Performance of Randomly Interleaved Prosaccades and Antisaccades
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NMDA Antagonist Ketamine Reduces Task Selectivity in Macaque Dorsolateral Prefrontal Neurons and Impairs Performance of Randomly Interleaved Prosaccades and Antisaccades

机译：NMDA拮抗剂氯胺酮降低猕猴背外侧前额神经元的任务选择性并损害随机交错的散步和反散步的性能。

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摘要

Ketamine, an NMDA receptor antagonist, has been shown to induce behavioral abnormalities in humans that mimic the positive, negative, and most importantly cognitive deficits observed in schizophrenia. Similar cognitive deficits have been observed in nonhuman primates after a subanesthetic dose of ketamine, including an impairment in their ability to perform the antisaccade task, which requires the suppression of a prosaccade toward a flashed stimulus and the generation of a saccade in the opposite direction. The neural basis underlying these cognitive impairments remains unknown. Here, we recorded single-neuron activity in the lateral prefrontal cortex of macaque monkeys before and after the administration of subanesthetic doses of ketamine during the performance of randomly interleaved prosaccade and antisaccade trials. Ketamine impeded the monkeys' ability to maintain and apply the correct task rule and increased reaction times of prosaccades and antisaccades. These behavioral changes were associated with an overall increase in activity of PFC neurons and a reduction in their task selectivity. Our results suggest that the mechanism underlying ketamine-induced cognitive abnormalities may be the nonspecific increase in PFC activity and the associated reduction of task selectivity.
机译：氯胺酮是一种NMDA受体拮抗剂，已被证明可诱导人类行为异常，从而模仿精神分裂症中观察到的阳性，阴性和最重要的认知缺陷。在非人灵长类氯胺酮麻醉后，在非人灵长类动物中也观察到类似的认知缺陷，包括其执行抗扫视任务的能力受损，这需要抑制向闪光刺激的扫视和沿相反方向扫视的产生。这些认知障碍的神经基础仍然未知。在这里，我们记录了在随机交错的前扫查和反扫查试验期间，在给予亚麻醉剂量的氯胺酮之前和之后，猕猴的外侧前额叶皮层中的单个神经元活性。氯胺酮阻碍了猴子维持和应用正确的任务规则的能力，并增加了s和反s的反应时间。这些行为改变与PFC神经元活动的总体增加和其任务选择性的降低有关。我们的结果表明，氯胺酮引起的认知异常的潜在机制可能是PFC活性的非特异性增加和相关的任务选择性降低。

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