Jaw S P, Hussong M J, Matsumoto R R, Truong D D
Department of Neurology, University of California Irvine, CA 92717.
Pharmacol Biochem Behav. 1994 Sep;49(1):129-31. doi: 10.1016/0091-3057(94)90466-9.
We have previously reported that rats exhibited audiogenic myoclonus at 3 days after cardiac arrest. This phenomenon peaked at 14 days, gradually tapered off at older ages, and disappeared in most rats by 60 days following cardiac arrest. Because treatment with the 5-HT2-selective agonist, (+/-)-1-2,5-dimethoxy-4-iodophenyl-2-aminopropane (DOI) significantly attenuated audiogenic myoclonus in these postcardiac-arrest rats, the involvement of 5-HT2 receptors in posthypoxic stimulus-sensitive myoclonus was suggested. In the current study, we, therefore, examined the binding properties of 5-HT2 receptors in the rat bain at various time points following cardiac arrest. The affinity constant of [3H]ketanserin binding to 5-HT2 receptors in cortical membranes of rats did not change. In contrast, Bmax values were found to be reduced at 3 and 14 days after cardiac arrest with some recovery after 60 days. Taken together with previous results, these results indicate that hypoactivity of central 5-HT2 neurotransmission may underlie the development of posthypoxic stimulus-sensitive myoclonus in rats.
我们之前报道过，大鼠在心脏骤停后3天会出现听源性肌阵挛。这种现象在14天时达到峰值，随着年龄增长逐渐减弱，在心脏骤停后60天时，大多数大鼠的该现象消失。因为用5-羟色胺2（5-HT2）选择性激动剂（±）-1-（2,5-二甲氧基-4-碘苯基）-2-氨基丙烷（DOI）治疗可显著减轻这些心脏骤停后大鼠的听源性肌阵挛，提示5-HT2受体参与了缺氧后刺激敏感性肌阵挛。因此，在本研究中，我们检测了心脏骤停后不同时间点大鼠脑内5-HT2受体的结合特性。大鼠皮质膜中[3H]酮色林与5-HT2受体结合的亲和常数没有变化。相反，发现心脏骤停后3天和14天Bmax值降低，60天后有所恢复。结合之前的结果，这些结果表明中枢5-HT2神经传递功能减退可能是大鼠缺氧后刺激敏感性肌阵挛发生的基础。
