【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。更多还原

【Abstract】 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.更多还原