Effects of Propofol on the Dynamic Properties of Sensory Information Processing in the Mouse Cerebellar Cortical Molecular Layer in vivo
Effects of Propofol on the Dynamic Properties of Sensory Information Processing in the Mouse Cerebellar Cortical Molecular Layer in vivo
复制标题
异丙酚对体内小鼠小脑皮质分子层感觉信息处理动态特性的影响
DOI：
10.1159/000441006
复制
发表时间：
2015-01-01
期刊：
影响因子：
3.1
通讯作者：
Qiu, De-Lai
中科院分区：
文献类型：
--
作者：
Jin, Wen-Zhe;Shi, Jin-Di;Qiu, De-Lai
异丙酚是一种影响中枢神经系统信息处理的全局中枢神经系统抑制剂。然而，异丙酚对小脑皮质分子层感觉信息处理的影响尚不清楚。在这项研究中，我们研究了异丙酚对感觉刺激诱发的反应在小脑分子层的动力学的影响，使用电生理和药理学方法。我们的结果表明，小脑表面灌注异丙酚（10- 1，000 μmol/l）显著降低感觉刺激诱发抑制成分（P1）的振幅和曲线下面积（AUC），但增加P1的上升时间和衰减时间。与此相反，丙泊酚的管理显着增强感觉刺激诱发的兴奋性成分（N1），表现出幅度和AUC的增加，以及上升时间和衰减时间的增加。通过阻断GABAA受体的活性，丙泊酚不能增加PC兴奋性突触后成分（N2）的振幅和AUC。我们目前的研究结果表明，异丙酚通过调节GABAA受体的活性，在成年小鼠小脑分子层的感觉信息处理的动态特性。
Propofol is a global central nervous system depressant that affects information processing in the central nervous system. However, the effects of propofol on sensory information processing in the cerebellar cortical molecular layer are unknown. In this study, we examined the effects of propofol on the dynamics of sensory stimulation-evoked responses in the cerebellar molecular layer in urethane-anesthetized mice, using electrophysiological and pharmacological methods. Our results showed that cerebellar surface perfusion of propofol (10-1,000 μmol/l) significantly decreased amplitude and area under the curve (AUC) of the sensory stimulation-evoked inhibitory component (P1) but increased the rise time and decay time of P1. In contrast, administration of propofol significantly enhanced the sensory stimulation-evoked excitatory component (N1), which exhibited increases in amplitude and AUC, as well as increases in rise time and decay time. By blocking the GABAA receptor activity, propofol failed to increase the amplitude and the AUC of the excitatory postsynaptic component (N2) of PCs. Our present results suggest that propofol modulates the dynamic properties of the sensory information processing in the cerebellar molecular layer through the modulation of GABAA receptors activity in the adult mouse.