Peterson S L
Department of Medical Pharmacology and Toxicology, Texas A&M University, College Station 77843.
Brain Res Bull. 1991 Jan;26(1):43-7. doi: 10.1016/0361-9230(91)90190-u.
This study evaluates the glycine potentiation of anticonvulsant drugs in subcutaneous pentylenetetrazol seizures in rats. Administered alone, glycine (30 or 40 mM/kg, PO) induced no anticonvulsant effect or neurological deficit. Coadministered with anticonvulsants, glycine significantly enhanced the anticonvulsant potency of diazepam and sodium valproate without affecting the neurological deficit induced by the anticonvulsants. Glycine did not significantly alter the anticonvulsant activity of ethosuximide or phenobarbital. These findings indicate a possible glycine-sensitive component in the mechanism of action of diazepam and sodium divalproate in subcutaneous pentylenetetrazol seizures. With the possible exception of sodium valproate, the present study provides little support for a glycine and gamma-aminobutyric acid (GABA) interaction as a mechanism of anticonvulsant activity in SC PTZ seizures. Further studies are required to determine the role of strychnine-sensitive and strychnine-insensitive glycine receptors in this experimental model of absence epilepsy.
本研究评估了甘氨酸对大鼠皮下注射戊四氮诱发癫痫发作时抗惊厥药物的增强作用。单独给予甘氨酸(30或40 mM/kg,口服)未产生抗惊厥作用或神经功能缺损。与抗惊厥药物联合给药时,甘氨酸显著增强了地西泮和丙戊酸钠的抗惊厥效力,且不影响抗惊厥药物所致的神经功能缺损。甘氨酸未显著改变乙琥胺或苯巴比妥的抗惊厥活性。这些发现表明,在皮下注射戊四氮诱发癫痫发作时,地西泮和丙戊酸钠的作用机制中可能存在对甘氨酸敏感的成分。除丙戊酸钠外,本研究几乎没有支持甘氨酸与γ-氨基丁酸(GABA)相互作用作为皮下注射戊四氮诱发癫痫发作时抗惊厥活性机制的证据。需要进一步研究以确定士的宁敏感和士的宁不敏感的甘氨酸受体在该失神癫痫实验模型中的作用。