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海马体的快速点燃可预防癫痫持续状态导致的神经损伤。

Rapid kindling of the hippocampus protects against neural damage resulting from status epilepticus.

作者信息

Penner M R, Pinaud R, Robertson H A

机构信息

Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada.

出版信息

Neuroreport. 2001 Mar 5;12(3):453-7. doi: 10.1097/00001756-200103050-00007.

Abstract

It has previously been reported that rats kindled via the standard kindling procedure do not exhibit the typical profile of neuropathology following status epilepticus. We wished to determine whether a 1-day rapid kindling procedure is also neuroprotective against cell damage resulting from prolonged seizure activity. We found that rats rapidly kindled from the dorsal hippocampus were more resistant to a kainic acid challenge 21-25 days after kindling than were unkindled control rats. Kindling prior to a kainic acid challenge also provided substantial protection against status epilepticus-induced damage in the CA3 region of the hippocampus and piriform cortex in most animals. Thus, despite the short kindling time period, rapid kindling is neuroprotective against status epilepticus-induced cell damage.

摘要

此前有报道称,通过标准点燃程序点燃的大鼠在癫痫持续状态后未表现出典型的神经病理学特征。我们希望确定1天快速点燃程序是否也对长时间癫痫活动导致的细胞损伤具有神经保护作用。我们发现,从背侧海马体快速点燃的大鼠在点燃后21 - 25天比未点燃的对照大鼠对 kainic 酸攻击更具抵抗力。在 kainic 酸攻击前进行点燃在大多数动物中也为海马体CA3区和梨状皮质中癫痫持续状态诱导的损伤提供了实质性保护。因此,尽管点燃时间短,但快速点燃对癫痫持续状态诱导的细胞损伤具有神经保护作用。

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