DISTURBANCE OF MEMBRANE-FUNCTION PRECEDING ISCHEMIC DELAYED NEURONAL DEATH IN THE GERBIL HIPPOCAMPUS
DISTURBANCE OF MEMBRANE-FUNCTION PRECEDING ISCHEMIC DELAYED NEURONAL DEATH IN THE GERBIL HIPPOCAMPUS
复制标题
DOI：
10.1038/jcbfm.1992.58
复制
发表时间：
1992-05-01
影响因子：
6.3
通讯作者：
KAWAI, N
中科院分区：
文献类型：
--
作者：
KIRINO, T;ROBINSON, HPC;KAWAI, N
用沙土鼠颈动脉夹闭法造成脑缺血5min后，取其海马作切片，观察锥体神经元的膜特性。大部分的CA1神经元失去了强直刺激后的输入纤维的长时程增强的能力。相反，CA3锥体神经元保留了与正常沙鼠相似的反应。缺血后，CA1锥体神经元表现出增加的自发放电，是高度电压依赖性的，并通过细胞内注射的钙离子螯合剂，EGTA被阻断。35%的CA1神经元在缺血24 h后出现异常的膜电位缓慢振荡。细胞内注射GTP-gamma-S或IP 3会促进振荡，然后出现不可逆的去极化。我们的研究结果表明，缺血损伤的CA1神经元遭受异常的Ca2+稳态，涉及IP3诱导的Ca2+从内部存储的释放。
Slice preparations were made from the hippocampus of gerbils after 5 min of ischemia by carotid artery occlusion and the membrane properties of pyramidal neurons were examined. A majority of CA1 neurons lost the capacity for long-term potentiation following tetanic stimulation of the input fibers. CA3 pyramidal neurons, in contrast, preserved responses similar to those in the normal gerbil. Following ischemia, CA1 pyramidal neurons showed increased spontaneous firing that was highly voltage dependent and was blocked by intracellular injection of the Ca2+ chelator, EGTA. Thirty-five percent of CA1 neurons showed an abnormal slow oscillation of the membrane potential after 24 h following ischemia. Intracellular injection of GTP-gamma-S or IP3 produced facilitation of the oscillations followed by irreversible depolarization. Our results indicate that ischemia-damaged CA1 neurons suffer from abnormal Ca2+ homeostasis, involving IP3-induced liberation of Ca2+ from internal stores.