Alvaro J D, Tatro J B, Quillan J M, Fogliano M, Eisenhard M, Lerner M R, Nestler E J, Duman R S
Laboratory of Molecular Psychiatry, Yale University School of Medicine, New Haven, Connecticut 06508, USA.
Mol Pharmacol. 1996 Sep;50(3):583-91.
Melanocortin peptides are reported to antagonize opiate dependence and tolerance, but the neural substrates underlying these actions are unknown. In this study, we characterize the rat melanocortin-4 receptor (MC4-R) and demonstrate that this receptor is regulated by opiate administration. The rat MC4-R is 95% identical to the human MC4-R, and the potency of melanocortin peptides to stimulate cAMP production is similar in these two species homologs (alpha-melanocyte-stimulating hormone = adrenocorticotropic hormone > gamma-melanocyte-stimulating hormone). Expression of MC4-R mRNA was found to be enriched in the striatum, nucleus accumbens, and periaque-ductal gray, all of which are regions implicated in the behavioral effects of opiates. In contrast, MC1-, MC3-, and MC5-R are expressed at very low or undetectable levels in these brain regions. Chronic administration of morphine (5 days) resulted in a time-dependent down-regulation of MC4-R mRNA expression in the striatum and periaqueductal gray. Expression of MC4-R mRNA was also decreased in the nucleus accumbens/ olfactory tubercle, but this effect was observed after 1 or 3 days of morphine treatment. In the striatum, the reduction of MC4-R mRNA was accompanied by a concomitant decrease in melanocortin receptor levels, shown by quantitative radioligand binding and autoradiography. In contrast, morphine administration did not influence levels of MC4-R mRNA in several other brain regions, including frontal cortex, olfactory bulb, hypothalamus, and ventral tegmentum/substantia nigra. In light of previous findings that melanocortins antagonize opiate self-administration, analgesic tolerance, and physical dependence, we hypothesize that decreased melanocortin function, via down-regulation of MC4-R expression, may contribute to the development of these opiate-induced behaviors.
据报道,促黑素细胞激素肽可拮抗阿片类药物依赖和耐受性,但其作用的神经基质尚不清楚。在本研究中,我们对大鼠促黑素细胞激素4受体(MC4-R)进行了表征,并证明该受体受阿片类药物给药的调节。大鼠MC4-R与人MC4-R有95%的同源性,在这两个物种同源物中,促黑素细胞激素肽刺激cAMP产生的效力相似(α-促黑素细胞激素=促肾上腺皮质激素>γ-促黑素细胞激素)。发现MC4-R mRNA在纹状体、伏隔核和导水管周围灰质中表达丰富,所有这些区域都与阿片类药物的行为效应有关。相比之下,MC1-R、MC3-R和MC5-R在这些脑区的表达水平非常低或无法检测到。慢性给予吗啡(5天)导致纹状体和导水管周围灰质中MC4-R mRNA表达随时间依赖性下调。伏隔核/嗅结节中MC4-R mRNA的表达也降低,但这种效应在吗啡治疗1或3天后观察到。在纹状体中,MC4-R mRNA的减少伴随着促黑素细胞激素受体水平的相应降低,这通过定量放射性配体结合和放射自显影显示。相比之下,吗啡给药不影响其他几个脑区的MC4-R mRNA水平,包括额叶皮质、嗅球、下丘脑和腹侧被盖区/黑质。鉴于先前的研究发现促黑素细胞激素可拮抗阿片类药物的自我给药、镇痛耐受性和身体依赖性,我们假设通过下调MC4-R表达导致的促黑素细胞激素功能降低可能有助于这些阿片类药物诱导行为的发展。