Taguchi K, Hagiwara Y, Suzuki Y
Department of Pharmacology, Showa College of Pharmaceutical Sciences, Tokyo, Japan.
Jpn J Pharmacol. 1991 Apr;55(4):453-9. doi: 10.1254/jjp.55.453.
We investigated the effects of beta-phenylethylamine (PEA) on photic-evoked potentials recorded from the cerebral cortex (visual cortex) in the anesthetized cat. The photic-evoked potential consisted of negative (N) and positive (P) components in the cerebral cortex, with peak times of 39.4 +/- 15.4 msec and 57.5 +/- 16.3 msec, respectively. Intravenous administration of PEA (6.5, 12.5 and 25 mg/kg) induced a dose-dependent decrease in the amplitude of the N component of photic-evoked potentials. PEA-induced decreases in the amplitude of photic-evoked potentials (at 12.5 mg/kg) were antagonized by yohimbine (2 mg/kg). Prazocin (2 mg/kg, i.v.) and propranolol (0.5 mg/kg, i.v.) did not change the PEA-induced decrease of photic-evoked potentials. Methysergide (2 mg/kg, i.v.), haloperidol (1 mg/kg, i.v.) and naloxone (0.5 mg/kg, i.v.) also failed to alter the inhibitory effect of PEA. Pretreatment with alpha-methyl-p-tyrosine or reserpine did not completely attenuate the PEA-induced decrease of photic-evoked potentials. According to these results, PEA inhibits the photic-evoked potentials in the visual cortex partially through the noradrenergic alpha 2-receptor.
我们研究了β-苯乙胺(PEA)对麻醉猫大脑皮层(视觉皮层)记录的光诱发电位的影响。光诱发电位在大脑皮层由负(N)和正(P)成分组成,峰值时间分别为39.4±15.4毫秒和57.5±16.3毫秒。静脉注射PEA(6.5、12.5和25毫克/千克)导致光诱发电位N成分的幅度呈剂量依赖性降低。育亨宾(2毫克/千克)可拮抗PEA(12.5毫克/千克)引起的光诱发电位幅度降低。哌唑嗪(2毫克/千克,静脉注射)和普萘洛尔(0.5毫克/千克,静脉注射)并未改变PEA引起的光诱发电位降低。甲基麦角新碱(2毫克/千克,静脉注射)、氟哌啶醇(1毫克/千克,静脉注射)和纳洛酮(0.5毫克/千克,静脉注射)也未能改变PEA的抑制作用。用α-甲基-p-酪氨酸或利血平预处理并未完全减弱PEA引起的光诱发电位降低。根据这些结果,PEA部分通过去甲肾上腺素能α2受体抑制视觉皮层的光诱发电位。