Gill R, Kemp J A
Merck Sharp and Dohme Research Laboratories, Neuroscience Research Centre, Harlow, U.K.
Neurosci Lett. 1989 Oct 23;105(1-2):101-6. doi: 10.1016/0304-3940(89)90019-0.
Electrophysiological recordings were made from hippocampal slices of gerbils which had undergone a 5 min period of bilateral carotid occlusion. Normal CA1 population spikes, field potentials and synaptic responses were obtained from slices of gerbils pretreated with the N-methyl-D-aspartate antagonist, MK-801 (10 mg/kg, i.p., 1 h before the occlusion). In contrast, no CA1 population spike could be obtained from slices of untreated gerbils, although field potentials and population spikes were obtained from the dentate granule cell region of these slices in response to perforant path stimulation. These studies indicate that the CA1 pyramidal cells identified histologically as protected by MK-801 from selective neuronal degeneration produced by a 5 min period of global ischaemia, are also functionally protected and retain their normal synaptic responsiveness.
对经历了5分钟双侧颈动脉闭塞的沙鼠海马切片进行电生理记录。在用N-甲基-D-天冬氨酸拮抗剂MK-801(10毫克/千克,腹腔注射,闭塞前1小时)预处理的沙鼠切片中获得了正常的CA1群体峰电位、场电位和突触反应。相比之下,未处理的沙鼠切片无法获得CA1群体峰电位,尽管在这些切片的齿状颗粒细胞区域对穿通通路刺激有场电位和群体峰电位。这些研究表明,组织学上确定为受MK-801保护免受5分钟全脑缺血所致选择性神经元变性影响的CA1锥体细胞,在功能上也受到保护并保留其正常的突触反应性。