Foong F W, Satoh M
Br J Pharmacol. 1984 Oct;83(2):493-7. doi: 10.1111/j.1476-5381.1984.tb16512.x.
Using freely moving and conscious rats, the antinociceptive effects of microinjections of carbamazepine, into the periaqueductal gray (PAG), nucleus reticularis paragigantocellularis (NRPG) and nucleus raphé magnus (NRM) on the biting-like responses induced by bradykinin applied to the tooth pulp, were investigated to determine the primary site of action of this drug. Microinjections of carbamazepine into the PAG ipsi- and contralateral to the stimulated tooth pulp produced dose-dependent suppressive effects on the biting-like responses within 1 min. The ED50 was 1.57 micrograms per rat, that is about 1,500 times less than that for carbamazepine administered systemically. The antinociceptive effect of carbamazepine administered into the PAG was inhibited by pretreatment with bicuculline but not by phentolamine, propranolol and haloperidol. Microinjections of carbamazepine into the NRPG and NRM were rarely effective in the production of antinociception at doses used (up to 3 micrograms per rat). These results suggest that the PAG is one of the primary target sites for the antinociceptive activity of carbamazepine, and that GABAergic systems are involved this action of carbamazepine.
利用自由活动且清醒的大鼠，研究了向中脑导水管周围灰质（PAG）、巨细胞旁网状核（NRPG）和中缝大核（NRM）微量注射卡马西平对应用于牙髓的缓激肽诱导的咬样反应的抗伤害感受作用，以确定该药物的主要作用部位。向受刺激牙髓同侧和对侧的PAG微量注射卡马西平在1分钟内对咬样反应产生剂量依赖性抑制作用。半数有效剂量（ED50）为每只大鼠1.57微克，约为全身给药时卡马西平ED50的1500分之一。向PAG注射卡马西平的抗伤害感受作用可被荷包牡丹碱预处理抑制，但不受酚妥拉明、普萘洛尔和氟哌啶醇抑制。在所用剂量（每只大鼠高达3微克）下，向NRPG和NRM微量注射卡马西平很少能产生抗伤害感受作用。这些结果表明，PAG是卡马西平抗伤害感受活性的主要靶点之一，且γ-氨基丁酸能系统参与了卡马西平的这一作用。
