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目的:研究碱中毒对小鼠皮质GABA能神经元内在特性和编码能力的影响,探讨碱中毒引起大脑功能障碍的机制。方法:选择17-22天FVB-Tg小鼠行脑片体外培养,实验对象分为碱中毒组和对照组。DIC光学显微镜下选择皮层II-III层GABA神经元,运用Axo Patch 200 B放大器全细胞模式,记录并分析神经元内在特性(包括阈电位、绝对不应期)的改变;记录与去极化脉冲相对应的峰值,分析GABA能神经元的编码能力。结果:1.阈电位峰值在对照组分别是24.58±0.68,25.44±0.82,27.02±0.78,27.55±0.74和28.66±0.79毫伏,碱中毒组分别是28.32±0.78,30.10±0.91,32.22±0.80,32.88±0.76和33.54±0.74毫伏,碱中毒组阈电位升高;绝对不应期在对照组和碱中毒组分别是4.15±0.06和5.09±0.08毫秒,碱中毒绝对不应期延长。2.两组在相同去极化刺激下诱发的连续峰值波形发生明显改变,碱中毒组产生峰值的能力下降。结论:1、碱中毒使皮质GABA能神经元动阈电位升高和绝对不应期延长;2、碱中毒降低皮质GABA能神经元编码峰值能力。
Objective: To investigate the effect of alkali poisoning on the intrinsic characteristics and coding ability of GABAergic neurons in mouse cortex and to explore the mechanism of brain dysfunction caused by alkali poisoning. Methods: FVB-Tg mice of 17-22 days were selected and cultured in vitro. The experimental subjects were divided into alkali poisoning group and control group. The GABA neurons in cortex II-III were selected under DIC optical microscope. The whole cell pattern of AxoPatch 200 B amplifier was used to record and analyze the changes of neuronal intrinsic characteristics (including threshold potential and absolute refractory period). The recording and depolarization pulse Corresponding peaks were analyzed for coding ability of GABAergic neurons. The peak value of threshold potentials were 24.58 ± 0.68, 25.44 ± 0.82, 27.02 ± 0.78, 27.55 ± 0.74 and 28.66 ± 0.79 millivolts in the control group and 28.32 ± 0.78, 30.10 ± 0.91 and 32.22 ± 0.80 , 32.88 ± 0.76 and 33.54 ± 0.74 millivolts respectively. The threshold potentials of alkaline poisoning group were increased. The absolute refractory period was 4.15 ± 0.06 and 5.09 ± 0.08 ms respectively in the control group and the alkali poisoning group. The absolute refractory period of alkali poisoning was prolonged. The continuous waveforms induced by the same depolarization changed significantly in both groups, and the ability of peak in alkali poisoning group decreased. Alkaline poisoning increased the threshold voltage and absolute refractory period of GABAergic neurons in cortex; 2, Alkaline poisoning reduced the peak capacity of coding GABAergic neurons in cortex.