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在长时间缺血后存活的大鼠中,背侧和腹侧海马体的Ca3神经元活动发生了不同程度的改变。

Ca3 neuronal activities of dorsal and ventral hippocampus are differentially altered in rats after prolonged post-ischemic survival.

作者信息

Wu C P, Cheung G, Rakhshani N, Parvardeh S, Asl M Nassiri, Huang H L, Zhang L

机构信息

Toronto Western Research Institute, University Health Network, Room 13-411, Toronto Western Hospital, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8.

出版信息

Neuroscience. 2005;130(2):527-39. doi: 10.1016/j.neuroscience.2004.09.041.

Abstract

The aim of the present study is to explore the potential hyper-excitability of hippocampal CA3 neurons in rats after prolonged post-ischemic survival. We conducted 15-min four-vessel-occlusion ischemic episodes in rats, allowed these animals to survive for approximately 8 months and then examined the basic morphological features and population synaptic activities of CA3 neurons. In fixed tissue sections obtained from dorsal hippocampi of post-ischemic rats, we observed a complete loss of the CA1 neurons together with a shrunken CA1 sector. Extracellular recordings in slices revealed that the overall synaptic activities of dorsal hippocampal CA3 neurons were decreased in post-ischemic rats compared with sham-operated controls. Both sham control and post-ischemic ventral hippocampal neurons were capable of exhibiting intermittent spontaneous field potentials in slices. These spontaneous field potentials spread from the CA3 to the CA1 area and their generation relied on the activity of glutamate alpha-amino-3-hydroxy-5-methyl-4 isoxazole proprionic acid (AMPA) receptors. The propensity for displaying these spontaneous field potentials appeared to be greater in post-ischemic slices than sham control slices. Our data suggest that the hyper-excitability of the post-ischemic hippocampus, if it occurs, may preferentially take place in the ventral CA3 circuitry.

摘要

本研究的目的是探讨大鼠缺血后长期存活后海马CA3神经元的潜在过度兴奋性。我们对大鼠进行了15分钟的四血管闭塞缺血发作,让这些动物存活约8个月,然后检查CA3神经元的基本形态特征和群体突触活动。在从缺血后大鼠背侧海马获得的固定组织切片中,我们观察到CA1神经元完全丧失以及CA1区萎缩。切片中的细胞外记录显示,与假手术对照组相比,缺血后大鼠背侧海马CA3神经元的整体突触活动降低。假手术对照组和缺血后腹侧海马神经元在切片中均能够表现出间歇性自发场电位。这些自发场电位从CA3扩散到CA1区,其产生依赖于谷氨酸α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体的活性。缺血后切片中显示这些自发场电位的倾向似乎比假手术对照组切片更大。我们的数据表明,缺血后海马的过度兴奋性(如果发生的话)可能优先发生在腹侧CA3神经回路中。

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