The effects of ketamine vary among inbred mouse strains and mimic schizophrenia for the P80, but not P20 or N40 auditory ERP components
The effects of ketamine vary among inbred mouse strains and mimic schizophrenia for the P80, but not P20 or N40 auditory ERP components
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DOI：
10.1023/b:nere.0000023605.68408.fb
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发表时间：
2004-06-01
影响因子：
4.4
通讯作者：
Siegel, SJ
中科院分区：
文献类型：
--
作者：
Connolly, PM;Maxwell, C;Siegel, SJ
N-甲基-D-天冬氨酸（NMDA）拮抗剂产生类似于精神分裂症的行为和电生理效应。小鼠P20，N40和P80事件相关电位（ERP）组件进行了分析，近交系之间的遗传变异和氯胺酮诱导的差异模型异常的P50，N100和P200精神分裂症。氯胺酮使P20/N40波幅增加，P80波幅降低。因此，氯胺酮在小鼠中的作用与精神分裂症中相应的P50和N100的改变不一致，表明NMDA受体功能障碍可能不是精神分裂症中这些成分异常的基础。然而，氯胺酮对小鼠P80的影响与精神分裂症的P200 ERP变化一致，并支持NMDA功能障碍可能导致精神分裂症的一些神经元异常的假设。目前的研究奠定了基础。研究NMDA介导的传递在神经元加工的特定方面的作用，这些方面随遗传背景而变化。未来的研究可以使用转录蛋白。林澄清遗传背景，特定的神经元回路和发射系统之间的这种相互作用。
N-methyl-D-aspartate (NMDA) antagonists produce behavioral and electrophysiological effects similar to schizophrenia. The mouse P20, N40, and P80 event related potential (ERP) components were analyzed for genetic variance among inbred strains and ketamine-induced differences to model abnormalities in the P50, N100, and P200 in schizophrenia. Ketamine increased P20/N40 amplitude and decreased P80 amplitude. Therefore, the effects of ketamine in mice are inconsistent with alterations in the corresponding P50 and N100 in schizophrenia, suggesting that NMDA receptor dysfunction may not underlie abnormalities of these components in schizophrenia. However, the effects of ketamine on the mouse P80 were consistent with P200 ERP changes in schizophrenia and support the hypothesis that NMDA dysfunction may contribute to some neuronal abnormalities in schizophrenia. The current study lays the groundwork for de. ning the role of NMDA-mediated transmission for specific aspects of neuronal processing that vary with genetic background. Future studies could use transcription pro. ling to clarify such interactions between genetic background, specific neuronal circuits, and transmitter systems.