【摘要】 目的 探讨γ-aminobutyric acid(GABA)及其受体拮抗剂对正常及脑缺血大鼠海马CA3区神经元突触传递功能的影响。方法在体记录正常大鼠海马CA3区诱发的群峰电(population spike,PS);结扎大鼠双侧颈总动脉,造成急性不完全性全脑缺血,观察PS幅度变化;采用局部微量给药,观察药物对PS幅度的影响。结果①GABA 100,200 mmol·L-1局部注入后,PS的幅度显著降低.bicuculline 1 mmol·L-1能明显拮抗GABA200 mmol·L-1对PS幅度降低的作用。②Glu 10 mmol·L-1注入后,PS的幅度较注药前显著增加。而Glu 50 mmol·L-1注入后,PS的幅度则较注药前显著降低。③GABA 200 mmol·L-1能显著降低Glu10 mmol·L-1所导致的PS幅度增加,并能减弱Glu 50 mmol·L-1对PS幅度的降低作用。④急性不完全性全脑缺血(结扎双侧颈总动脉)后,PS的幅度显著降低。GABA 200 mmol·L-1能减轻脑缺血所致的PS幅度的降低。结论 GABA对正常大鼠海马神经元突触传递的兴奋性具有一定抑制作用。并能明显改善较大剂量谷氨酸和急性脑缺血对海马CA3区神经元突触传递的影响。更多还原

【Abstract】 OBJECTIVE To observe the effects of γ-GABA on evoked potential(population spike, PS) in the hippocampus CA3 region after brain ischemia.METHODS Transient incomplete global brain ischemia was caused by occluding both carotid arteries.Intracellular recording was used to study the amplitude of PS of hippocampus CA3 area in vivo. RESULTS The animal received a GABA intra-hippocampal infusion of 100 mmol·L-1 and 200 mmol·L-1, respectively. Both GABA-treated groups had a dose-dependent decrease of the PS amplitude at all measured time points(0,10,20,30,40,50,60 min).Bicuculline 1 mmol·L-1 antagonised the action of 200 mmol·L-1 GABA.Glu 10 mmol·L-1 increased PS amplitude.But Glu 50 mmol·L-1 significantly decreased the amplitude of PS.GABA 200 mmol’L suppressed both the effects of Glu 10 mmol·L-1 and Glu 50 mmol·L-1.After both carotid arteries was occluded to cause incomplete global brain ischemia, the, amplitude of PS decreased significantly. GABA 200 mmol·L-1 attenuated the depression effect of ischemia. CONCLUSION The results suggest that GABA plays an important regulative role in the changes of synaptic transmission induced by EAA and brain ischemia in rata.更多还原