Araki T, Kato H, Kogure K, Saito T
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
J Neurol Sci. 1991 Dec;106(2):206-12. doi: 10.1016/0022-510x(91)90259-a.
We performed receptor autoradiography to determine sequential alterations in the binding of muscarinic cholinergic and adenosine A1 receptors and of a voltage dependent L-type calcium channel blocker 1 h-1 month after transient cerebral ischemia in the gerbil brain. [3H]Quinuclidinyl benzilate (QNB), [3H]cyclohexyladenosine (CHA) and [3H]PN200-110 were used to label muscarinic and adenosine A1 receptors and L-type calcium channels, respectively. Transient ischemia was induced for 10 min. [3H]QNB and [3H]CHA binding showed no significant alteration in selectively vulnerable areas at an early stage (1-24 h) of recirculation. However, the dentate molecular layer which was resistant to ischemia revealed a significant decrease in the [3H]CHA binding sites 24 h after ischemia. Thereafter, the [3H]QNB and [3H]CHA binding showed significant reduction in most of selectively vulnerable areas. Marked reduction was especially found in the dorsolateral part of striatum and the hippocampal CA1 sector which was the most vulnerable to ischemia. In contrast, [3H]PN200-110 binding showed a transient elevation in the hippocampal CA1 sector, the dentate molecular layer and the thalamus 1 h of recirculation. However, the striatum and neocortex revealed no alteration in the [3H]PN200-110 binding. Thereafter, the reduction in the [3H]PN200-110 binding was seen only in the dorsolateral part of the striatum and the hippocampal CA1 sector. The results suggest that transient cerebral ischemia can cause the alterations in the binding of muscarinic cholinergic and adenosine A1 receptors and of L-type calcium channel blocker in most of selectively vulnerable areas.(ABSTRACT TRUNCATED AT 250 WORDS)
我们进行了受体放射自显影,以确定沙土鼠脑短暂性脑缺血后1小时至1个月期间,毒蕈碱胆碱能受体、腺苷A1受体以及电压依赖性L型钙通道阻滞剂结合的顺序变化。[3H]奎宁环基苯甲酸酯(QNB)、[3H]环己基腺苷(CHA)和[3H]PN200-110分别用于标记毒蕈碱受体、腺苷A1受体和L型钙通道。短暂性缺血诱导10分钟。在再灌注早期(1-24小时),[3H]QNB和[3H]CHA结合在选择性易损区域无显著变化。然而,对缺血有抵抗性的齿状分子层在缺血后24小时显示[3H]CHA结合位点显著减少。此后,[3H]QNB和[3H]CHA结合在大多数选择性易损区域显著降低。在纹状体背外侧部分和对缺血最敏感的海马CA1区尤其发现明显降低。相比之下,[3H]PN200-110结合在再灌注1小时时,在海马CA1区、齿状分子层和丘脑短暂升高。然而,纹状体和新皮层的[3H]PN200-110结合无变化。此后,仅在纹状体背外侧部分和海马CA1区观察到[3H]PN200-110结合减少。结果表明,短暂性脑缺血可导致大多数选择性易损区域毒蕈碱胆碱能受体、腺苷A1受体以及L型钙通道阻滞剂结合的变化。(摘要截断于250字)