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[目的]探讨乙醇对小鼠小脑皮层浦肯野细胞(PC)复杂性峰电位(CS)活动的影响.[方法]取6~8周龄昆明种小鼠,腹腔注射给予乌拉坦(1.3g/kg)施行麻醉,在小脑Vermis区施行直径为1.0~1.5mm的开颅术,揭除硬脑膜,在暴露的脑表面区域持续灌流给予含氧的人工脑脊液(ACSF);电生理记录选用在体膜片钳记录,并结合生物素染色技术,记录电极内充装20~30μL电极內液,阻抗为4~6 MΩ;通过膜片钳放大器及数据采集软件记录小脑皮层PC自发性活动.[结果]给予乌拉坦施行麻醉后,小鼠小脑皮层Vermis区PC表现为规律的单纯性峰电位(SS)放电,平均频率为(19.00±4.20)Hz;同时伴有不规律的CS活动,平均频率为(0.31±0.12)Hz;在电流钳记录模式下,乙醇(300 mmol/L)可缩短放电暂停时间,减少后超极化振幅;在电压钳下,乙醇可显著抑制CS的小穗个数及波形下面积,但对CS发生频率即小穗间隔频率未见有影响;乙醇对CS的抑制作用具有一定的剂量依存性;阻断NMDA和mGluR1受体对乙醇所起的CS抑制作用未见有影响,但乙醇对CS的抑制作用可被CB1受体阻断剂所阻断.[结论]乙醇通过活化CB1受体抑制小鼠小脑皮层PC的CS活动,提示过量饮酒可能通过激活攀缘纤维-PC突触前CB1受体抑制外周信息向小脑皮层PC的传入,进而影响运动调节功能.
[Objective] To investigate the effect of ethanol on the activity of Purkinje cell (PC) complex peak potential (CS) in mouse cerebellar cortex. [Methods] Kunming mice of 6-8 weeks old were injected intraperitoneally with urethane / kg), a craniotomy with a diameter of 1.0 to 1.5 mm was performed in the Vermis area of the cerebellum, the dura mater was removed and continuous oxygenation of artificial cerebrospinal fluid (ACSF) was performed in the exposed brain surface area. Electrophysiological recording was performed on Body patch clamp recording, combined with biotin staining, the recording electrode filled with 20 ~ 30μL electrode solution, the impedance of 4 ~ 6 MΩ; through the patch clamp amplifier and data acquisition software to record the cerebellar cortex PC spontaneous activity [ Results] After administration of urethane, PC in the mouse cerebellar cortex Vermis showed a regular simple peak potential (SS) discharge with an average frequency of (19.00 ± 4.20) Hz. Meanwhile, irregular CS activity accompanied with an average frequency (0.31 ± 0.12) Hz. In current clamp recording mode, ethanol (300 mmol / L) shortened the discharge pause time and decreased the amplitude of post-hyperpolarization. Under the voltage clamp, ethanol significantly inhibited the number of spikelets And the area under the waveform, but no impact on the frequency of CS spikelet frequency; ethanol inhibition of CS The effect of ethanol on CS was blocked by blocking the NMDA and mGluR1 receptors on the inhibitory effect of ethanol on CS.CONCLUSIONS: Ethanol can inhibit CS activity in mouse cerebellar cortex PC by activating CB1 receptor, suggesting that excessive alcohol consumption may inhibit the afferent function of peripheral information to PC of cerebellar cortex by activating the CB1 receptor of climbing fiber-PC.