【摘要】 目的　探讨谷氨酸及其受体拮抗剂对正常和脑缺血大鼠海马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区诱发的群峰电位 (populationspike,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幅度的变化 ;采用局部微量给药 ,观察药物对PS幅度的影响。结果　①Glu 5、1 0、2 0nmol注入后 ,PS的幅度均升高 ;当给予Glu 5 0nmol时PS的幅度则显著降低。②急性不完全性全脑缺血 (结扎双侧颈总动脉 )后 ,PS的幅度亦显著降低。③谷氨酸受体拮抗剂MK 80 1 5 0nmol能降低正常大鼠的PS幅度 ,能部分改善脑缺血引起的PS幅度降低 ,并能减弱 1 0nmolGlu升高PS幅度的作用和 5 0nmolGlu降低PS幅度的作用。结论　谷氨酸在一定浓度范围内可增强大鼠海马CA3区的突触传递功能 ,其受体拮抗剂MK 80 1对高浓度谷氨酸和急性脑缺血所致CA3区突触传递功能减弱有明显的改善作用。更多还原

【Abstract】 AIM In this electrophysiological study, we observed the effects of glutamic acid and its receptor antagonist on synaptic transmission in hippocampus CA3 region of normal and ischemic rats. METHODS The evoked population spike(PS) was recorded in hippocampus CA3 region of normal rats in vivo ; Transient incomplete global brain ischemia was caused by occluding both carotid arteries, and the change of PS amplitudes were observed; Drugs were injected locally in microdose and their effects on PS amplitudes were observed. RESULTS (1) Animals were given a Glu intra hippocampal infusion of 5,10 and 20 nmol, respectively. The results showed a increase of the amplitudes of PS at all measured time points (5,10,20,30,40,50,60 min), but Glu 50 nmol significantly decreased the amplitudes of PS. (2) After both carotid arteries had been occluded to cause incomplete global brain ischemia, the amplitudes of PS decreased significantly. (3) MK 801 50 nmol decreased the PS amplitudes of normal rat, but partly ameliorated the depressive effect of ischemia, it also suppressed the effect of 10 nmol Glu and the effect of 50 nmol Glu. CONCLUSION In an range of dose, glutamic acid enhanced synaptic transmission in hippocampus CA3 region, and its receptor antagonist MK 801 significantly ameliorated the depressive effects of higher dose glutamic acid and ischemia on synaptic transmission in hippocampus CA3 region.更多还原