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短暂的癫痫发作活动可保护大鼠大脑免受癫痫持续状态诱导的神经元损伤。

A short episode of seizure activity protects from status epilepticus-induced neuronal damage in rat brain.

作者信息

Najm I M, Hadam J, Ckakraverty D, Mikuni N, Penrod C, Sopa C, Markarian G, Lüders H O, Babb T, Baudry M

机构信息

Department of Neurology, The Cleveland Clinic Foundation, Cleveland, OH, USA.

出版信息

Brain Res. 1998 Nov 9;810(1-2):72-5. doi: 10.1016/s0006-8993(98)00886-5.

Abstract

Kainic acid (KA)-induced status epilepticus (SE) in adult rats results in extensive neuronal damage throughout the limbic system and the loss of selectively vulnerable neuronal populations, particularly CA3 neurons. We investigated the effects of a short episode of seizure activity on neuronal death elicited by a subsequent prolonged SE episode. A short episode of seizure activity was produced by sub-cutaneous (s.c.) injection of KA followed after 1 h by pentobarbital administration. Twenty-four hours later, KA was administered again, and animals were sacrificed 3 days later. Neuronal damage was estimated by visual analysis of neuronal density. Our results show that a short episode of seizure activity did not produce neuronal damage but almost completely protected vulnerable neurons from KA-induced neuronal damage. These results extend to epileptic tolerance the notion of tolerance previously described in the case of ischemia.

摘要

成年大鼠注射海人酸(KA)诱发癫痫持续状态(SE)会导致整个边缘系统广泛的神经元损伤以及选择性易损神经元群体的丧失,尤其是CA3神经元。我们研究了短时间癫痫发作活动对随后长时间SE发作所引发的神经元死亡的影响。通过皮下(s.c.)注射KA产生短时间癫痫发作活动,1小时后给予戊巴比妥。24小时后再次注射KA,3天后处死动物。通过视觉分析神经元密度来评估神经元损伤。我们的结果表明,短时间癫痫发作活动并未产生神经元损伤,反而几乎完全保护了易损神经元免受KA诱导的神经元损伤。这些结果将先前在缺血情况中描述的耐受性概念扩展到了癫痫耐受性。

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