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机构地区:[1]田纳西大学医学院神经病学系,第一军医大学生理学教研室
出 处:《神经解剖学杂志》1996年第4期361-370,共10页Chinese Journal of Neuroanatomy
基 金:中国国家自然科学基金
摘 要:脑缺血在在体大鼠海马CA1锥体神经元上诱发出一种NMDA受体介导的新突触后电位高天明(GaoTianming)徐造成(XuZaocheng)(田纳西大学医学院神经病学系,盂菲斯,田纳西38104美国;第一军医大学生理学教研室,广州510515)海马C...Abstract Pyramidal neurons in the CA1 field of the hippocampus die a few days after transient cerebral ischemia. Excessive excitatory synaptic activation following reperfusion is thought to be responsible for such delayed cell death. However, itremains controversial whether excitatory synaptic.transmission in the CA1 field is increased following reperfusion. To understand the electrophysiological mechanisms associated with postischemic neuronal injury, the present study investigated thechanges of synaptic transmission and passive neuronal properties of CA1 pyramidal neurons in the postischemic period usingintracellular recording and staining techniques in vivo.Male Wistar rats were fasted overnight and anesthetized with 1~2% halothane mixed with 33% O2 and 66% N2. The arterial gas tension and other physiological parameters of the animal were monitored during the experiment. The brain temperature was maintained at 37℃ during ischemia. Severe forebrain ischemia was induced by four-vessel occlusion for about 15min. Postsynaptic potentials(PSPs) were elicited by stimulation of contralateral commissural pathway (CC). The spontaneous firing, PSPs and membrane properties of CA1 neurons were compared before and after ischemia. The recorded neurons were identified by intracellular staining with neurobiotin.In animals after reper fusion, CC stimuli elicited a late depolarizing postsynaptic potential (L-PSP) in addition to the initialEPSP from 60% (87/144)of CA1 neurons recorded within two days after ischemia. The L-PSP couldn't be evoked by injection of depolarizing current pulses, indicating that it is not an intrinsic regenerating membrane properties but a synapticallydriven event. Action potentials occasionally arose from the L-PSP and the estimated reversal potential of L-PSP was -55mV, suggesting that it is an EPSP. According to the input-output curves of initial EPSP and L-PSP, the stimulus intensityrequired to evoke responses of 50% maximal amplitude from these two components was different(1. 5 times threshold f
关 键 词:脑缺血 海马 NMDA受体 突触后电位 锥体神经元
分 类 号:R743.310.2[医药卫生—神经病学与精神病学]
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