Weiss S R, Post R M, Marangos P J, Patel J
Neuropharmacology. 1985 Jul;24(7):635-8. doi: 10.1016/0028-3908(85)90105-4.
This study investigates the ability of adenosine antagonists to reverse the anticonvulsant effects of carbamazepine on amygdala-kindled seizures in order to elucidate the possible physiological relevance of the potent effects of carbamazepine on adenosine receptors. At large but subconvulsant doses, neither caffeine nor theophylline altered the anticonvulsant potency of carbamazepine, even though caffeine by itself significantly increased the duration of the kindled afterdischarge. The adenosine agonist cyclohexyladenosine (CHA), administered intraperitoneally at a dose that produced sedation, had no effect on the kindled seizures. Although carbamazepine potently displaces the binding of several adenosine ligands in vitro, the present data do not suggest that the anticonvulsant effects of carbamazepine on amygdalakindled seizures are mediated by an adenosine agonist-like action.
本研究调查腺苷拮抗剂逆转卡马西平对杏仁核点燃性癫痫发作的抗惊厥作用的能力,以阐明卡马西平对腺苷受体强效作用的可能生理相关性。在大剂量但亚惊厥剂量下,咖啡因和茶碱均未改变卡马西平的抗惊厥效力,尽管咖啡因本身显著增加了点燃后放电的持续时间。腹腔注射产生镇静作用剂量的腺苷激动剂环己基腺苷(CHA)对点燃性癫痫发作没有影响。虽然卡马西平在体外能有效取代几种腺苷配体的结合,但目前的数据并不表明卡马西平对杏仁核点燃性癫痫发作的抗惊厥作用是由腺苷激动剂样作用介导的。