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完整及皮层下结构损伤大鼠的戊四氮(PTZ)点燃发展过程

Pentylenetetrazol (PTZ)-kindling development in intact and subcortical structure lesioned rats.

作者信息

Bandyopadhyay A

出版信息

Indian J Exp Biol. 1989 Sep;27(9):829-30.

PMID:2632405
Abstract

Kindling was induced in male wistar rats (280-320 g) by daily ip injections of PTZ in subthreshold doses (30 mg/kg). Repeated administration of PTZ to animals resulted in developing of enhanced seizures and also enhanced seizure susceptibility which could be sustained for a long time (6 months) after last seizure paroxysm. The lesioned hippocampus retarded the manifestation of PTZ kindling, where as lesioned caudate nuclei increased the seizure kindling development. Results also revealed hippocampus as a determinant structure in PTZ kindling formation, which stabilize the epileptic manifestations and make them chronic, at the same time caudate nuclei retarded the epileptic seizures stabilization. This role may be only antiepileptic, and not anti-kindling as is known for caudate nuclei.

摘要

通过每天腹腔注射阈下剂量的戊四氮(PTZ,30毫克/千克)诱导雄性Wistar大鼠(体重280 - 320克)产生点燃效应。对动物反复给予PTZ会导致癫痫发作增强以及癫痫易感性增强,这种易感性在最后一次癫痫发作后很长一段时间(6个月)内都可持续存在。受损的海马体延缓了PTZ点燃效应的表现,而受损的尾状核则加速了癫痫点燃效应的发展。结果还表明,海马体是PTZ点燃效应形成中的决定性结构,它使癫痫表现稳定并使其慢性化,同时尾状核延缓了癫痫发作的稳定。这种作用可能仅仅是抗癫痫的,而不像尾状核那样具有抗点燃作用。

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