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氨基甲酸乙酯麻醉抑制海马亚阈活动和神经元同步。

Urethane anesthesia suppresses hippocampal subthreshold activity and neuronal synchronization.

机构信息

Graduate School of Pharmaceutical Sciences, University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo 113-0033, Japan.

Graduate School of Pharmaceutical Sciences, University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo 113-0033, Japan; Center for Information and Neural Networks, Suita City, Osaka 565-0871, Japan.

出版信息

Brain Res. 2020 Dec 15;1749:147137. doi: 10.1016/j.brainres.2020.147137. Epub 2020 Sep 29.

Abstract

Urethane, an anesthetic utilized for animal experiments, induces neocortical slow oscillations in which a large number of neurons emit rhythmic synchronized activity. However, it remains unclear how urethane affects neuronal activity in the hippocampus. In this study, we obtained in vivo patch-clamp recordings from dorsal hippocampal CA1 neurons in mice and found a reduction in the fluctuation of subthreshold membrane potentials during urethane anesthesia, implying reduced synaptic activity in the hippocampus. We then performed spike unit recordings from dorsal hippocampal CA1 neuronal ensembles in rats and found prominent reductions in the spike rates of the majority of hippocampal units, especially spatially selective units, during urethane anesthesia, whereas a subset of nonspatial units exhibited increased spike rates. The overall reductions in neuronal spike rates induced by urethane led to prominent decreases in spike synchronization across neuronal units. Consistently, the magnitude of hippocampal sharp wave ripples was also reduced by urethane. The suppression of hippocampal neuronal synchronization by urethane may lead to the disruption of offline memory reactivation mechanisms.

摘要

氨基甲酸乙酯,一种用于动物实验的麻醉剂,诱导新皮层慢波振荡,其中大量神经元发出有节奏的同步活动。然而,氨基甲酸乙酯如何影响海马体中的神经元活动仍不清楚。在这项研究中,我们从小鼠背侧海马 CA1 神经元获得了体内膜片钳记录,发现氨基甲酸乙酯麻醉期间阈下膜电位的波动减少,这意味着海马体中的突触活动减少。然后,我们从大鼠背侧海马 CA1 神经元集合体中进行了尖峰单位记录,发现大多数海马体单位的尖峰率在氨基甲酸乙酯麻醉期间明显降低,特别是空间选择性单位,而一部分非空间单位的尖峰率增加。氨基甲酸乙酯诱导的神经元尖峰率的总体降低导致神经元单位之间的尖峰同步明显降低。一致地,海马体尖锐波涟漪的幅度也被氨基甲酸乙酯降低。氨基甲酸乙酯对海马体神经元同步的抑制可能导致离线记忆再激活机制的破坏。

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