Schoffelmeer A N, Hansen H A, Stoof J C, Mulder A H
Eur J Pharmacol. 1985 Dec 3;118(3):363-6. doi: 10.1016/0014-2999(85)90150-5.
The cyclic AMP efflux from rat neostriatal slices induced by simultaneous activation of D-1 (stimulatory) and D-2 (inhibitory) dopamine receptors with 30 microM dopamine was inhibited by morphine (0.3-3 microM), [D-Ala2, D-Leu5]enkephalin (DADLE, 0.03-0.3 microM) but not by [D-Pen2, D-Pen5]enkephalin (DPDPE, 0.03-0.3 microM). The inhibitory effects were abolished by naloxone (0.1 microM). Upon selective D-1 dopamine receptor activation with 30 microM dopamine in the presence of 10 microM of the D-2 dopamine receptor antagonist (-)sulpiride, the enhanced efflux of cyclic AMP was reduced by all three opioid receptor agonists, but only the effect of morphine was antagonized by 0.1 microM naloxone. These data suggest that the cyclic AMP production induced in rat neostriatum by simultaneous D-1 and D-2 dopamine receptor activation may be inhibited through mu-opioid receptors, whereas on blockade of D-2 dopamine receptors both mu- and delta-opioid receptors may be linked to adenylate cyclase in an inhibitory fashion.
用30微摩尔多巴胺同时激活D-1(刺激性)和D-2(抑制性)多巴胺受体所诱导的大鼠新纹状体切片中环磷酸腺苷(cAMP)外流,被吗啡(0.3 - 3微摩尔)、[D-丙氨酸2,D-亮氨酸5]脑啡肽(DADLE,0.03 - 0.3微摩尔)抑制,但不被[D-青霉胺2,D-青霉胺5]脑啡肽(DPDPE,0.03 - 0.3微摩尔)抑制。这些抑制作用被纳洛酮(0.1微摩尔)消除。在用30微摩尔多巴胺选择性激活D-1多巴胺受体且存在10微摩尔D-2多巴胺受体拮抗剂(-)舒必利的情况下,所有三种阿片受体激动剂均降低了cAMP增强的外流,但只有吗啡的作用被0.1微摩尔纳洛酮拮抗。这些数据表明,同时激活D-1和D-2多巴胺受体在大鼠新纹状体中诱导产生的cAMP可能通过μ-阿片受体被抑制,而在阻断D-2多巴胺受体时,μ-和δ-阿片受体可能以抑制方式与腺苷酸环化酶相联系。