Gylys K H, Tran N, Magendzo K, Zaki P, Evans C J
Department of Psychiatry and Biobehavioural Sciences, UCLA-NPI 90024-1759, USA.
Neuroreport. 1997 Jul 7;8(9-10):2369-72. doi: 10.1097/00001756-199707070-00053.
We have compared several drug combinations for their ability to increase basal cAMP and to down-regulate delta-opioid receptor mRNA levels. Continuous treatment for up to 48 h with a phosphodiesterase inhibitor in combination with the adenylyl cyclase activator forskolin showed an early peak response, but cAMP levels returned to control after 8 and 24 h. Increases in cAMP level up to 150-fold were observed after treatment for 1 h with a series of drugs (rolipram, IBMX/forskolin, rolipram/forskolin, dibutyryl cAMP, and prostaglandin E2) that increase cAMP by different mechanisms. A significant decrease in DOR mRNA level, to 31% of control, followed the three treatments that produced the largest increases in cAMP level: IBMX/forskolin, rolipram/forskolin, and prostaglandin E2.
我们比较了几种药物组合增加基础环磷酸腺苷(cAMP)以及下调δ-阿片受体mRNA水平的能力。用磷酸二酯酶抑制剂与腺苷酸环化酶激活剂福斯高林连续处理长达48小时,显示出早期峰值反应,但cAMP水平在8小时和24小时后恢复到对照水平。用一系列通过不同机制增加cAMP的药物(咯利普兰、异丁基甲基黄嘌呤/福斯高林、咯利普兰/福斯高林、二丁酰环磷腺苷和前列腺素E2)处理1小时后,观察到cAMP水平增加高达150倍。在导致cAMP水平最大增加的三种处理(异丁基甲基黄嘌呤/福斯高林、咯利普兰/福斯高林和前列腺素E2)之后,DOR mRNA水平显著下降至对照水平的31%。