Brailowsky S, Montiel T, Meneses S, Di Scala G
Departamento de Neurociencias, Universidad Nacional Autónoma de México. sbrailow@ifcsun 1.ifisiol.unam.mx
Brain Res. 1995 Dec 8;702(1-2):126-32. doi: 10.1016/0006-8993(95)01033-x.
The acute effects of two GABAB receptor antagonists (phaclofen and CGP-35348) were studied in two types of epileptogenic activity: that produced by intracortical injections of baclofen and that appearing after withdrawal of chronic intracerebral GABA infusion (the GABA-withdrawal syndrome, GWS). Intracortical baclofen induced two types of electrographic paroxysmal discharges: one consisting of single spike-and-wave (pattern I) and another of polyspike-and-wave patterns (pattern II). Both patterns showed similar latencies and temporal evolution of spike frequency discharges. Phaclofen, applied directly into the baclofen-induced epileptogenic focus, suppressed pattern II but was ineffective in modifying both pattern I and the GWS. CGP-35348, administered systemically, inhibited both patterns I and II. Intracortical microinjection of baclofen or phaclofen in rats showing a GWS had no effect, nor the systematically given CGP 35348. These results indicate a differential participation of GABAB receptors in GABA-related epileptic syndromes of cortical origin.
研究了两种GABAB受体拮抗剂(巴氯芬和CGP-35348)对两种致痫活性的急性作用:一种是由皮质内注射巴氯芬产生的致痫活性,另一种是慢性脑室内GABA输注撤除后出现的致痫活性(GABA撤除综合征,GWS)。皮质内注射巴氯芬诱发了两种类型的脑电图阵发性放电:一种由单个棘波和慢波组成(模式I),另一种由多棘波和慢波模式组成(模式II)。两种模式的放电潜伏期和频率随时间的变化相似。直接注入巴氯芬诱发的致痫灶中的巴氯芬,可抑制模式II,但对模式I和GWS均无影响。全身给药的CGP-35348可抑制模式I和模式II。在出现GWS的大鼠中,皮质内微量注射巴氯芬或巴氯芬均无作用,全身给药的CGP 35348也无作用。这些结果表明,GABAB受体在皮质起源的GABA相关癫痫综合征中具有不同的参与情况。