吗啡对大鼠尾壳核神经元阿片受体基因表达的影响

目的探讨较长时间给予吗啡对体外培养大鼠尾壳核神经元的μ、δ型阿片受体mRNA表达的影响。方法采用逆转录-聚合酶链反应(RT-PCR)方法。结果吗啡可使μ、δ型阿片受体的mRNA水平显著降低(P<0.01),吗啡作用12h、24h和48h可使μ型阿片受体mRNA由0h时的94.8%分别降至50%、42.7%和67.2%;而对δ型阿片受体,则只有在24h和48h有明显的抑制作用(P<0.01),由0h时的95.8%分别降至59.5%和84.5%;吗啡在10-8mol/L时即可引起μ型阿片受体的mRNA水平显著降低,且该抑制效应在10-8mol/L^10-5mol/L浓度范围内呈明显的剂量依赖性,但对δ型阿片受体则在10-6mol/L时才有效。结论吗啡较长时间作用于原代培养大鼠尾壳核神经元,可明显抑制μ、δ型阿片受体的基因表达。

EFFECTS OF SEVERAL RGSS ON ADENYLATE CYCLASE (AC) ASSOCIATED WITH MU AND DELTA OPIOD-RECEPTORS

The cycle of G-protein activation and deactivation is a key in the signaling pathway of GPCRs (G protein coupled receptors). GTPase-activating proteins (GAPs) regulate heterotrimeric G proteins by increasing the rates at which the (subunits hydrolyze bound GTP to GDP. RGSs (regulators of G protein signaling) is a novel family and, in most cases, implicated in accelerating the hydrolysis of GTP. The opioid receptors are all seven serpentine transmembrane receptors coupled with G proteins Gi, Go, even Gs. Adenylate cyclase (AC) is