Lucchi L, Rius R A, Govoni S, Trabucchi M
Alcohol. 1985 Mar-Apr;2(2):193-5. doi: 10.1016/0741-8329(85)90044-8.
Ethanol induces supersensitivity of striatal delta-opiate receptor sites labelled by 3H-Etorphine. This effect may be ascribed to the diminished enkephalin release detected in striatal slices after chronic ethanol consumption. On the other hand, Kd values for 3H-Met-enkephalin and 3H-DHM (mu-opiate receptors) specific binding are enhanced. The different sensitivity of the two classes of opiate receptors to ethanol may be due to specific effects on enkephalinergic transmission. It has been hypothesized that the decrease of 3H-Met-enkephalin and 3H-DHM affinity for their receptors takes place because endogenous substances from ethanol metabolism (for example salsolinol) behave as mu opioid agonists. This hypothesis is confirmed by "in vitro" studies demonstrating that salsolinol displaces 3H-Met-enkephalin and 3H-DHM but not 3H-DADLE binding. On the contrary, it seems that delta-receptors become supersensitive because of the decreased endogenous peptide release.
乙醇可诱导纹状体中由³H-埃托啡标记的δ-阿片受体位点超敏。这种效应可能归因于长期摄入乙醇后纹状体切片中检测到的脑啡肽释放减少。另一方面，³H-甲硫氨酸脑啡肽和³H-DHM（μ-阿片受体）特异性结合的解离常数增加。两类阿片受体对乙醇的不同敏感性可能是由于对脑啡肽能传递的特定影响。据推测，³H-甲硫氨酸脑啡肽和³H-DHM与其受体亲和力的降低是因为乙醇代谢产生的内源性物质（如萨索林醇）表现为μ阿片受体激动剂。“体外”研究证实了这一假设，该研究表明萨索林醇可取代³H-甲硫氨酸脑啡肽和³H-DHM，但不能取代³H-DADLE的结合。相反，δ-受体似乎因内源性肽释放减少而变得超敏。
