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脑损伤诱导的边缘系统癫痫发生增强:与颞叶癫痫动物模型的解剖学和生理学相似性

Brain injury-induced enhanced limbic epileptogenesis: anatomical and physiological parallels to an animal model of temporal lobe epilepsy.

作者信息

Coulter D A, Rafiq A, Shumate M, Gong Q Z, DeLorenzo R J, Lyeth B G

机构信息

Department of Neurology, Medical College of Virginia, Richmond 23298-0599, USA.

出版信息

Epilepsy Res. 1996 Dec;26(1):81-91. doi: 10.1016/s0920-1211(96)00044-7.

DOI:10.1016/s0920-1211(96)00044-7
PMID:8985690
Abstract

Traumatic brain injury (TBI) is a leading cause of symptomatic epilepsy in young adults. This study examined physiological and anatomical epileptogenic consequences of a prior incident of TBI in rats. Rats were subjected to a fluid percussion brain injury one week prior to experimentation, and in vitro electrophysiological recording studies were conducted using combined hippocampal-entorhinal cortical slices (HEC slices). Results were compared to sham operated controls and rats in which a condition of chronic temporal lobe epilepsy was induced by a 2 h bout of pilocarpine-induced status epilepticus 2 months prior to recording (PILO). In field potential recording, PILO HEC slices evidenced a greater degree of disinhibition in Ca1 than did TBI or control slices. TBI slices showed greater disinhibition in the dentate gyrus than did PILO or control rats. In in vitro kindling experiments, 86% of TBI HEC slices generated self-sustaining epileptic activity within 9 stimulus trains. This type of activity was never triggered in control slices. HEC slices prepared from PILO animals generated self-sustaining epileptic activity with fewer stimulus trains than did TBI slices. In anatomical studies, both TBI and PILO hippocampi evidenced significant loss of neurons within the hilar region. TBI induces a series of changes within the limbic system of rats, which are qualitatively similar in many aspects but quantitatively less severe than changes seen in rats with chronic temporal lobe epilepsy. These physiological and anatomical TBI-associated alterations in the limbic system may contribute to the development of epilepsy following head trauma.

摘要

创伤性脑损伤(TBI)是年轻成年人症状性癫痫的主要病因。本研究考察了大鼠既往TBI事件的生理和解剖学致痫后果。在实验前一周,对大鼠进行液压冲击性脑损伤,使用海马-内嗅皮质联合切片(HEC切片)进行体外电生理记录研究。将结果与假手术对照组以及在记录前2个月通过2小时匹罗卡品诱导的癫痫持续状态诱发慢性颞叶癫痫的大鼠(PILO)进行比较。在场电位记录中,PILO HEC切片在Ca1区的去抑制程度比TBI或对照组切片更大。TBI切片在齿状回的去抑制程度比PILO或对照大鼠更大。在体外点燃实验中,86%的TBI HEC切片在9次刺激序列内产生了自持性癫痫活动。这种活动在对照切片中从未触发。从PILO动物制备的HEC切片产生自持性癫痫活动所需的刺激序列比TBI切片少。在解剖学研究中,TBI和PILO海马在门区均出现了明显的神经元丢失。TBI在大鼠边缘系统内诱发了一系列变化,这些变化在许多方面在性质上相似,但在数量上比慢性颞叶癫痫大鼠所见的变化轻。这些与TBI相关的边缘系统生理和解剖学改变可能有助于头部创伤后癫痫的发生。

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