Treatment of rats with N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) resulted in a pronounced loss of alpha 2-adrenoceptor binding ( [3H]RX-781094) and a marked reduction in the ability of the alpha 2-agonist UK-14,304 to inhibit K+-stimulated release of both [3H]NA and [3H]5-HT in cerebral cortex. Repopulation of alpha 2-adrenoceptors was monoexponential with a t1/2 of 4.1 days; functional recovery was also monoexponential, with t1/2 values of 2.4 and 4.6 days for restoration of alpha 2-mediated inhibition of [3H]NA and [3H]5-HT release, respectively. Other studies suggest the difference in functional recovery rate may reflect the presence of a large receptor reserve for autoreceptors relative to heteroreceptors.

译文

用N-ethoxycarbonyl-2-ethoxy-1,2-二氢喹啉 (EEDQ) 治疗大鼠导致 α2-肾上腺素受体结合的明显丧失 ([3H]RX-781094) 和 α2-激动剂UK-14的能力显着降低,304抑制K刺激的 [3H]NA和 [3H]5-HT在大脑皮层中的释放。α2-肾上腺素受体的再增加是单指数的,t1/2为4.1天; 功能恢复也是单指数的,分别用2.4和4.6天的t1/2值来恢复 α2介导的 [3H]NA和 [3H]5-HT释放的抑制。其他研究表明功能治愈率的差异可能反映了相对于异受体而言自身受体储备较大的存在。

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