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黄 丽, 王 春, 李 言, 等.酸中毒对小鼠大脑皮层GABA能神经元电生理特性的影响.四川大学学报(医学版),2018,49(3):342-346
酸中毒对小鼠大脑皮层GABA能神经元电生理特性的影响
Influence of Acidosis on Electrophysiological Characteristics of Cortical GABAergic Neurons in Mice
  
中文关键词:  酸中毒 GABA能神经元 动作电位 突触传递 膜片钳全细胞记录
英文关键词:Acidosis GABAergic neurons Action potential Synaptic transmission Patch clamp whole cell recording
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中文摘要:
      目的 探讨胞外酸中毒对小鼠大脑皮层γ-氨基丁酸(GABA)能神经元动作电位发放和突触传递功能的影响。方法 选择出生后27~30 d的小鼠20只,做大脑冠状切片,随后分为正常对照组和细胞外酸中毒组:大脑冠状切片灌流pH值为7.4的人工脑脊液,采用膜片钳全细胞电流钳模式记录动作电位阈电位、绝对不应期和动作电位峰间距,电压钳模式记录自发性兴奋性突触后电流,为正常对照组;随后将灌流人工脑脊液的pH值调为6.5,模拟胞外酸中毒,为细胞外酸中毒组。再次记录神经元动作电位和自发性兴奋性突触后电流,比较两组间以上各项指标的差异。结果 与正常对照组对比,胞外酸中毒使GABA能神经元动作电位峰间距和绝对不应期延长(P<0.01),阈电位升高(P<0.01),自发性兴奋性突触后电流幅度和频率增加(P<0.01)。结论 胞外酸中毒损伤大脑皮层GABA能神经元动作电位的发放和突触传递,这可能是酸中毒诱导脑功能损伤的机制之一。
英文摘要:
      Objective To investigate the influences of extracellular acidosis on spike encoding and synaptic transmission of cortical GABAergic neurons in mice. Methods Twenty mice aged 27-30 d mice were selected to prepare coronary cortical slices and then divided into control group and extracellular acidosis group. In control group, the coronal slices were perfused with artificial cerebrospinal fluid at pH7.4, the action potential threshold potential, absolute refractory period and action potential peak spacing were recorded with the patch-clamp all-cell current clamp mode; the spontaneous excitatory postsynaptic current was recorded with the voltage clamp mode extracellular acidosis group, the artificial cerebrospinal fluid was adjusted at pH6.5, mimicking extracellular acidosis. Recorded neurons action potential and spontaneous excitatory postsynaptic currents again, comparing the difference of the above indexes between the two groups. Results Compared with the control group, the extracellular acidosis significantly prolonged the inter-spike intervals and absolute refractory periods (P<0.01), increased the voltage of threshold potentials and the amplitude and frequency of spontaneous excitatory postsynaptic currents (P<0.01). Conclusion Extracellular acidosis leads to the dysfunction of cortical GABAergic neurons by breaking the inter-characteristics and synaptic transmission, contributing one of the possible mechanisms to acidosis-induced brain damage.
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