Jaw S P, Dang T, Truong D D
Parkinson and Movement Disorders Laboratory, Department of Neurology, University of California Irvine 92717, USA.
Pharmacol Biochem Behav. 1995 Nov;52(3):577-80. doi: 10.1016/0091-3057(95)00143-k.
Following 10 min cardiac arrest and resuscitation, male Sprague-Dawley rats developed posthypoxic myoclonus. This phenomenon peaked at 14 days and disappeared by 60 days after cardiac arrest. From previous results, the 5-hydroxytryptamine (5-HT) system was implicated in the pathogenesis of the disease. In the present study, we investigated the involvement of 5-HT1A receptors in posthypoxic myoclonus in rats. Single injections of 5-HT1A agonists, buspirone (5 and 10 mg/kg body wt.) or 8-OH-DPAT (1, 2, and 4 mg/kg), had no effect on either the intensity or time course of the disease. In contrast, multiple injections (twice a day for 7 or more days) of buspirone (10 mg/kg) or 8-OH-DPAT (4 mg/kg) significantly attenuated the myoclonus scores of animals (p < 0.05). The results indicate that chronic stimulation of 5-HT1A receptors in the brain may accelerate endogenous compensatory mechanisms and shorten the time course of the disease.
在经历10分钟心脏骤停和复苏后，雄性Sprague-Dawley大鼠出现了缺氧后肌阵挛。这种现象在心脏骤停后14天达到峰值，并在60天后消失。根据先前的研究结果，5-羟色胺（5-HT）系统与该疾病的发病机制有关。在本研究中，我们调查了5-HT1A受体在大鼠缺氧后肌阵挛中的作用。单次注射5-HT1A激动剂，丁螺环酮（5和10mg/kg体重）或8-OH-DPAT（1、2和4mg/kg），对疾病的强度或病程均无影响。相比之下，多次注射（每天两次，持续7天或更长时间）丁螺环酮（10mg/kg）或8-OH-DPAT（4mg/kg）可显著降低动物的肌阵挛评分（p<0.05）。结果表明，大脑中5-HT1A受体的慢性刺激可能会加速内源性代偿机制，并缩短疾病的病程。
