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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。
To explore the biochemical mechanism of epilepsy. Methods The function of hippocampal somatostatin (SOM) receptors in chronic epileptic rats induced by pentylenetetrazole was assayed using 125I-SOM as a ligand and radioligand receptor binding assay. Results The Bmax values of hippocampal SOM receptors in chronic epilepsy rats and controls were 246.0 ± 18.2 pmol / g protein and 220.0 ± 15.3 pmol / g protein, respectively, with Kd values of 4.19 ± 0.34 nmol / L and 3.89 ± 0.22nmol / L. The commonly used antiepileptic agents carbamazepine (CBZ), sodium valproate (VPA) and calcium antagonist nimodipine (NIM) reduced receptor affinity, whereas phenytoin sodium (PHT) had no effect. Conclusion The increased activity of SOM receptor plays an important role in the pathogenesis of epilepsy. The antiepileptic activity of commonly used antiepileptic drugs may be related to the decrease of SOM receptor activity.