Nicotine modulates the facial stimulation-evoked responses in cerebellar granule cell layer in vivo in mice.
Nicotine modulates the facial stimulation-evoked responses in cerebellar granule cell layer in vivo in mice.
复制标题
尼古丁调节小鼠体内小脑颗粒细胞层的面部刺激诱发的反应。
DOI：
10.1016/j.ejphar.2018.11.022
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发表时间：
2019
影响因子：
5
通讯作者：
Qiu De-Lai
中科院分区：
文献类型：
--
作者：
Xu Yin-Hua;Zhang Bin-Bin;Su Wen-Hao;Wu Mao-Cheng;Bing Yan-Hua;Cui Song-Biao;Chu Chun-Ping;Li Yu-Zi;Qiu De-Lai
烟碱型乙酰胆碱受体是中枢神经系统中介导快速兴奋性传递的阳离子通道。在小脑颗粒细胞层（GCL）中检测到几种烟碱型乙酰胆碱受体亚单位，这些受体的激活可能对小脑神经元突触传递产生重要影响。本研究的目的是更好地了解烟碱型乙酰胆碱受体在小脑GCL的感觉刺激诱发的突触传递中的作用。我们的研究结果表明，小脑表面灌注尼古丁显着促进小脑GCL场电位反应所引起的同侧胡须垫，这表现出增加的幅度和曲线下面积的刺激起始反应（N1）和刺激偏移反应（N2）。尼古丁诱导的面部刺激诱发的N1 AUC增加呈剂量依赖性，50%有效浓度（EC50）为32.6 μM。单独应用选择性α4β2烟碱乙酰胆碱受体拮抗剂DHβE（1 μM）或选择性α7烟碱乙酰胆碱受体拮抗剂MLA（1 μM）可减弱但不能完全消除尼古丁诱导的面部刺激诱发的N1振幅和AUC增加。然而，同时阻断α7和α4β2烟碱乙酰胆碱受体亚基可消除尼古丁诱导的N1振幅增加。这些结果表明，尼古丁激活α7和α4β2烟碱乙酰胆碱受体亚基，导致小鼠小脑GCL中面部刺激诱发的反应增强。我们的研究结果表明，尼古丁通过α7和α4β2亚基烟碱乙酰胆碱受体调节小脑GCL的感觉信息处理。
Nicotinic acetylcholine receptors are cationic channels that mediate fast excitatory transmission in the central nervous system. Several nicotinic acetylcholine receptor subunits have been detected within cerebellar granule cell layer (GCL), and activation of these receptors may have a significant influence on neuronal synaptic transmission of the cerebellum. The aim of present study was to better understand the roles of nicotinic acetylcholine receptors during the sensory stimulation-evoked synaptic transmission in the cerebellar GCL. Our results showed that cerebellar surface perfusion of nicotine significantly facilitated the cerebellar GCL field potential responses evoked by air-puff stimulation of ipsilateral whisker pad, which exhibited increases in amplitude and area under the curve (AUC) of both stimulus onset responses (N1) and stimulus offset responses (N2). The nicotine-induced increase in AUC of facial stimulation-evoked N1 was dose-dependent with a 50% effective concentration (EC50) of 32.6 μM. Application of either a selective α4β2 nicotinic acetylcholine receptors antagonist, DHβE (1 μM) or a selective α7 nicotinic acetylcholine receptors antagonist, MLA (1 μM) alone attenuated, but not completely abolished the nicotine-induced increases in the amplitude and AUC of the facial stimulation-evoked N1. However, simultaneous blockade of α7 and α4β2 nicotinic acetylcholine receptor subunits abolished the nicotine-induced increase in the amplitude of N1. These results indicate that nicotine activates α7 and α4β2 nicotinic acetylcholine receptor subunits, resulting in an enhancement of facial stimulation-evoked responses in mouse cerebellar GCL. Our results suggest that nicotine modulates the sensory information processing in the cerebellar GCL through α7 and α4β2 subunits nicotinic acetylcholine receptors.