汪银洲 阮旭中 章军建 430030 武汉 同济医科大学同济医院神经内科 中风与神经疾病杂志 1999 0 16 1


    关键词：生长抑素；受体；戊四氮；慢性癫痫；大鼠 期刊 zfysjjbzz 0 论著与经验总结 fur -->


    

摘 要 目的 探讨癫痫发病的生化机制。方法 用¹²⁵ I-SOM作为配基，采用放射性配基受体结合分析法，对戊四氮诱导的慢性癫痫大鼠海马生长抑素(SOM)受体功能进行了测定。结果 慢性癫痫大鼠及对照组海马SOM受体的Bmax值分别为246.0±18.2pmol/g蛋白质及220.0±15.3pmol/g蛋白质，Kd值分别为4.19±0.34nmol/L及3.89±0.22nmol/L。常用的抗痫药卡马西平(CBZ)、丙戊酸钠(VPA)及钙拮抗剂尼莫地平(NIM)能降低受体的亲和力，而苯妥因钠(PHT)则无影响。结论 SOM受体活性增高在癫痫发病中起着重要作用，常用抗痫药的抗痫活性可能与其降低SOM受体活性有关。

Somatostatin receptorfunction is enhanced in

    the hippocampus of pentylenetetrazol-induced chronic epileptic rats

WangYinzhou,Ruan Xuzhong,Zhang Junjian.

    Department of Neurology,Tongji Hospital,Tongji Medical University,Wuhan 430030

Abstract Objective To explore the biochemicalpathogenesis of epilepsy. Methods The functional activity of somatostatin (SOM) receptor wasexamined in hippocampus of pentylenetetrazol-induced chronic epileptic rats by means ofradioligand binding assay. Binding to SOM receptor was studied using ¹²⁵ I-SOM as radioligand.Results Amaximal binding capacity (Bmax) of 246.0±18.2pmol/g of protein and a dissociationconstant (Kd) of 41.9±0.34 nmol/L in hippocampus of experimental rats were obviouslyincreased as compared with controls. (Bmax=220.0±15.3pmol/g of protein,Kd=3.89±0.22nmol/L).The carbamazepine,valproic acid and nimodipine were effective in significantly inhibitingbinding whereas phenytoin no effective. Conclusions The increase in SOM receptor activity may contribute tothe pathogenesis of epilepsy.

    Key Words Somatostatin Receptor Pentylenetetrazol Chronic epilepsy Rat

生长抑素(Somatostatin,SOM)作为一种神经递质或调质 ......

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