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氯胺酮改变海马中的振荡耦合。

Ketamine alters oscillatory coupling in the hippocampus.

机构信息

Brain Institute, Federal University of Rio Grande do Norte, Natal, RN 59056-450, Brazil.

出版信息

Sci Rep. 2013;3:2348. doi: 10.1038/srep02348.

DOI:10.1038/srep02348
PMID:23907109
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3731648/
Abstract

Recent studies show that higher order oscillatory interactions such as cross-frequency coupling are important for brain functions that are impaired in schizophrenia, including perception, attention and memory. Here we investigated the dynamics of oscillatory coupling in the hippocampus of awake rats upon NMDA receptor blockade by ketamine, a pharmacological model of schizophrenia. Ketamine (25, 50 and 75 mg/kg i.p.) increased gamma and high-frequency oscillations (HFO) in all depths of the CA1-dentate axis, while theta power changes depended on anatomical location and were independent of a transient increase of delta oscillations. Phase coherence of gamma and HFO increased across hippocampal layers. Phase-amplitude coupling between theta and fast oscillations was markedly altered in a dose-dependent manner: ketamine increased hippocampal theta-HFO coupling at all doses, while theta-gamma coupling increased at the lowest dose and was disrupted at the highest dose. Our results demonstrate that ketamine alters network interactions that underlie cognitively relevant theta-gamma coupling.

摘要

最近的研究表明,高阶振荡相互作用(如交叉频率耦合)对于精神分裂症中受损的大脑功能(包括感知、注意和记忆)很重要。在这里,我们研究了在 NMDA 受体阻断剂氯胺酮(一种精神分裂症的药理学模型)作用下,清醒大鼠海马体中振荡耦合的动力学。氯胺酮(25、50 和 75 mg/kg,ip)增加了 CA1-齿状回轴的所有深度的伽马和高频振荡(HFO),而θ功率变化取决于解剖位置,且与短暂的δ振荡增加无关。γ和 HFO 的相位相干性在海马体各层中增加。θ和快速振荡之间的相位-幅度耦合以剂量依赖性的方式显著改变:氯胺酮在所有剂量下增加海马体θ-HFO 耦合,而θ-γ 耦合在最低剂量下增加,并在最高剂量下被破坏。我们的研究结果表明,氯胺酮改变了网络相互作用,这些相互作用是与认知相关的θ-γ 耦合的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/b4cc7bd529be/srep02348-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/944e6fa3bea6/srep02348-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/548cd0ed4c84/srep02348-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/c801250ed11b/srep02348-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/91e0359129e3/srep02348-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/1929442b4382/srep02348-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/8c48ed0db830/srep02348-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/bf93988aea9d/srep02348-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/b4cc7bd529be/srep02348-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/944e6fa3bea6/srep02348-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/548cd0ed4c84/srep02348-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/c801250ed11b/srep02348-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/91e0359129e3/srep02348-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/1929442b4382/srep02348-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/8c48ed0db830/srep02348-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/bf93988aea9d/srep02348-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7693/3731648/b4cc7bd529be/srep02348-f8.jpg

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OLM interneurons differentially modulate CA3 and entorhinal inputs to hippocampal CA1 neurons.
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