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首页> 外文期刊>CNS neuroscience & therapeutics. >Impact of Ketamine on Neuronal Network Dynamics: Translational Modeling of Schizophrenia‐Relevant Deficits
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Impact of Ketamine on Neuronal Network Dynamics: Translational Modeling of Schizophrenia‐Relevant Deficits

机译：氯胺酮对神经元网络动力学的影响：精神分裂症相关缺陷的转化模型。

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Summary Subanesthetic doses of the psychomimetic, ketamine, have been used for many years to elicit behavioral effects reminiscent of schizophrenia in both healthy humans and in animal models of the disease. More recently, there has been a move toward the use of simple neurophysiological measures (event‐related potentials, brain oscillations) to assay the functional integrity of neuronal circuits in schizophrenia as these measures can be assessed in patients, healthy controls, intact animals, and even in brain slices. Furthermore, alterations of these measures are correlated with basic information processing deficits that are now considered central to the disease. Thus, here we review recent studies that determine the effect of ketamine on these measures and discuss to what extent they recapitulate findings in patients with schizophrenia. In particular, we examine methodological differences between human and animal studies and compare in vivo and in vitro effects of ketamine. Ketamine acts on multiple cortical and subcortical sites, as well as on receptors other than the N ‐methyl‐ d ‐aspartate receptor. Acute ketamine models' changes correlated with psychotic states (e.g. increased baseline gamma‐band oscillations), whereas chronic ketamine causes cortical circuit changes and neurophysiological deficits (e.g. impaired event‐related gamma‐band oscillations) correlated with cognitive impairments in schizophrenia.
机译：小结拟态药物氯胺酮的亚麻醉剂量已被使用多年，以在健康的人和该疾病的动物模型中引起让人联想到精神分裂症的行为效应。最近，人们开始使用简单的神经生理学方法（事件相关电位，脑震荡）来分析精神分裂症中神经元回路的功能完整性，因为这些方法可以在患者，健康对照，完整动物和即使在脑片中。此外，这些措施的改变与目前被认为是疾病的主要信息处理缺陷有关。因此，在这里，我们回顾了最近的研究，这些研究确定了氯胺酮对这些措施的影响，并讨论了他们在多大程度上概括了精神分裂症患者的发现。特别是，我们检查了人类和动物研究之间的方法学差异，并比较了氯胺酮的体内和体外作用。氯胺酮作用于多个皮质和皮质下位点，以及除N-甲基-d-天冬氨酸受体以外的受体上。急性氯胺酮模型的变化与精神状态有关（例如基线γ-波段振荡增加），而慢性氯胺酮会引起皮层回路变化和神经生理缺陷（例如事件相关的γ-波段振荡受损）与精神分裂症的认知障碍有关。

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