摘要
探讨癫痫发病的生化机制。方法用１２５Ｉ－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）、丙戌酸钠（ＶＰＡ）及钙桔抗剂尼莫地平（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。
Objective To explore the biochemical pathogenesis of epilepsy. Methods The functional activity of somatostatin (SOM) receptor was examined in hippocampus of pentylenetetrazol-in-duced chronic epileptic rats by means of radioligand binding assay. Binding to SOM receptor was studiedusing 125I-SOM as radioligand. Results A maximal binding capacity (Bmax) of 246.0±18. 2pmol/g ofprotein and a dissociation constant (Kd) of 41.9±0. 34 nmol/L in hippocampus of experimental ratswere obviously increased as compared with controls. (Bmax=220.0±15. 3pmol/g of protein, Kd=3. 89±0. 22nmol/L). The carbamazepine,valproic acid and nitnodipine were effective in significantly inhibiting binding whereas phenytoin no effective. Conclusions The increase in SOM receptor activity maycontribute to the pathogenesis of epilepsy.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
1999年第1期24-26,共3页
Journal of Apoplexy and Nervous Diseases
基金
国家自然科学基金!No39330210
关键词
生长抑素
受体
戊四氮
慢性
癫痫
大鼠
Somatostatin Receptor Pentylenetetrazol Chronic epilepsy Rat
