Kulkarni S K, George B
Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India.
Indian J Exp Biol. 1995 Jun;33(6):424-7.
Repeated administration of pentylenetetrazol (PTZ, 30 mg/kg, thrice a week) to mice for 9 weeks and subsequent challenge of the animals with the same dose of PTZ on the last chronic dose produced chemical kindling. The mice showed myoclonic jerks, clonus, Straub's tail, falling back response and full blown convulsions. The anticonvulsant profile of chronic administration of BR-16A (100 and 500 mg/kg) was studied in this model of epilepsy. BR-16A offered protection against PTZ-induced chemical kindling. The per cent animals showing myoclonic jerks and clonus was reduced to 40 and 34 with 100 mg/kg and 54 and 27 with 500 mg/kg of BR-16A, respectively. The protective effect was compared with diazepam (1 mg/kg, ip). The results demonstrated GABAA receptor mediated PTZ-induced kindling and protective effect of BR-16A therein.
对小鼠每周三次重复给予戊四氮(PTZ,30毫克/千克),持续9周,然后在末次长期给药时用相同剂量的PTZ对动物进行激发,从而产生化学性点燃。小鼠表现出肌阵挛性抽搐、阵挛、施特劳布尾、后仰反应和全面惊厥。在该癫痫模型中研究了长期给予BR-16A(100和500毫克/千克)的抗惊厥作用。BR-16A对PTZ诱导的化学性点燃具有保护作用。分别给予100毫克/千克和500毫克/千克BR-16A时,出现肌阵挛性抽搐和阵挛的动物百分比分别降至40%和34%,以及54%和27%。将其保护作用与地西泮(1毫克/千克,腹腔注射)进行比较。结果证明了GABAA受体介导的PTZ诱导的点燃以及BR-16A在其中的保护作用。