Francis A, Fochtmann L
Department of Psychiatry, SUNY Stony Brook 11794, USA.
Psychopharmacology (Berl). 1995 May;119(1):99-104. doi: 10.1007/BF02246060.
A variety of neurotransmitter receptor changes occur after a course of electroconvulsive seizures (ECS) in rats, including an increased density of adenosine A1 sites. Adenosine antagonism has been related to the proconvulsant action of methylxanthines such as caffeine. We determined tonic-clonic seizure duration in rats given ECS with caffeine (0-175 mg/kg, IP) after a course of one or six daily ECS. A single day of ECS did not affect the dose-dependent proconvulsant action of caffeine. After six daily ECS, the proconvulsant action of caffeine was reduced. After nine daily ECS, an A1 antagonist (8-cyclopentyl-1,3-dipropylxanthine) and an A2A antagonist (1-allyl-3,7-dimethyl-8-p-sulfophenylxanthine) showed reduced proconvulsant activity. The results suggest that the reduced proconvulsant action of caffeine after chronic ECS depends on adenosine antagonism.
在大鼠经历一个疗程的电惊厥发作(ECS)后,会发生多种神经递质受体变化,包括腺苷A1位点密度增加。腺苷拮抗作用与咖啡因等甲基黄嘌呤的促惊厥作用有关。我们测定了在经历一或六个每日疗程的ECS后,给予咖啡因(0 - 175毫克/千克,腹腔注射)的大鼠强直阵挛性发作持续时间。单日ECS不影响咖啡因的剂量依赖性促惊厥作用。在六个每日疗程的ECS后,咖啡因的促惊厥作用降低。在九个每日疗程的ECS后,A1拮抗剂(8 - 环戊基 - 1,3 - 二丙基黄嘌呤)和A2A拮抗剂(1 - 烯丙基 - 3,7 - 二甲基 - 8 - 对 - 磺基苯基黄嘌呤)的促惊厥活性降低。结果表明,慢性ECS后咖啡因促惊厥作用的降低取决于腺苷拮抗作用。