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[急性惊厥后大鼠小脑苯二氮䓬受体的特性及氯氮卓诱导点燃的发展]

[The properties of the benzodiazepine receptors in the rat cerebellum after acute seizures and the development of korazol-induced kindling].

作者信息

Bazian A S, Zhulin V V, Karpova M N, Klishina N Iu, Glebov R N

机构信息

Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow.

出版信息

Zh Vyssh Nerv Deiat Im I P Pavlova. 1998 Jan-Feb;48(1):135-42.

PMID:9583173
Abstract

The acute korazol (pentylenetetrazol) injection (50 mg/kg) induced seizures which were accompanied by a long-lasting (from 30 minutes to 3 days) decrease in benzodiazepine receptor (BDR) density (Bmax) in rat cerebellum without change in affinity. The density of the BDR was normalized on the 7th day after seizure termination. There were no differences in the initial BDR characteristics between the animals more sensitive to korazol (a dose of 25 mg/kg was sufficient for seizure induction) and less sensitive (30 mg/kg were ineffective). The chronic daily (for 24 days) administration of korazol in a subconvulsive dose led to an increase in seizure readiness (kindling). In 30 min after the last korazol injection the BDR density was decreased to the same extent as after the acute 50 mg/kg korasol administration. The BDR density was normalized on the 7th day after kindling. It was demonstrated that the high-dose-induced and after-kindling seizures were underlain by the same mechanisms. The results suggest that the development of kindling depends on the state of the long-lasting receptors rather than the development of kindling forms the long-lasting reactions. The process of summation is at the basis of kindling development. The long-lasting decrease in activity of BDR receptors induced by a subconvulsive dose of korazol is summed with the following effect of the same dose.

摘要

急性注射氯氮卓(戊四氮)(50毫克/千克)诱发癫痫发作,同时大鼠小脑苯二氮䓬受体(BDR)密度(Bmax)出现持续较长时间(30分钟至3天)的下降,而亲和力不变。癫痫发作终止后第7天,BDR密度恢复正常。对氯氮卓更敏感的动物(25毫克/千克剂量足以诱发癫痫发作)和较不敏感的动物(30毫克/千克无效)之间,初始BDR特征没有差异。以亚惊厥剂量每日(共24天)慢性给予氯氮卓会导致癫痫发作易感性增加(点燃效应)。在最后一次注射氯氮卓后30分钟,BDR密度下降程度与急性给予50毫克/千克氯氮卓后相同。点燃效应后第7天,BDR密度恢复正常。结果表明,高剂量诱发的癫痫发作和点燃效应后的癫痫发作具有相同的机制。结果提示,点燃效应的发展取决于长效受体的状态,而非点燃效应形成长效反应。总和过程是点燃效应发展的基础。亚惊厥剂量的氯氮卓诱导的BDR受体活性的长期下降与相同剂量的后续效应相加。

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