Pilc A, Vetulani J, Nomura S, Enna S J
Institute of Pharmacology, Polish Academy of Sciences, Krakow.
Brain Res. 1989 Jul 24;493(1):8-13. doi: 10.1016/0006-8993(89)90994-3.
Intraperitoneal administration of 0.8 mg/kg N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) to rats significantly reduced alpha-adrenoceptor binding in cerebral cortical membranes without affecting beta-adrenoceptor sites. A selective reduction in alpha 1-adrenoceptors was achieved by injecting yohimbine prior to EEDQ, whereas prazosin pretreatment yielded a selective reduction in alpha 2-adrenoceptor binding. Administration of EEDQ decreased norepinephrine-stimulated inositol phosphate and cyclic adenosine monophosphate (cAMP) accumulation in cerebral cortical tissue as well as the cAMP response to isoproterenol in combination with 6-fluoronorepinephrine without modifying the second messenger response to isoproterenol alone. The results suggest that, under the proper conditions, EEDQ administration can selectively diminish rat brain alpha-adrenoceptor number and function, yielding a procedure that may be useful for defining the behavioral and physiological properties of these sites.
给大鼠腹腔注射0.8毫克/千克的N - 乙氧羰基 - 2 - 乙氧基 - 1,2 - 二氢喹啉（EEDQ）可显著降低大脑皮质膜中的α - 肾上腺素能受体结合，而不影响β - 肾上腺素能受体位点。在注射EEDQ之前注射育亨宾可实现α1 - 肾上腺素能受体的选择性减少，而哌唑嗪预处理则导致α2 - 肾上腺素能受体结合的选择性减少。EEDQ的给药降低了去甲肾上腺素刺激的大脑皮质组织中肌醇磷酸和环磷酸腺苷（cAMP）的积累，以及与6 - 氟去甲肾上腺素联合使用时对异丙肾上腺素的cAMP反应，而不改变单独对异丙肾上腺素的第二信使反应。结果表明，在适当条件下，给予EEDQ可选择性减少大鼠脑α - 肾上腺素能受体数量和功能，产生一种可能有助于定义这些位点的行为和生理特性的方法。
