Oron L, Sarne Y, Michaelson D M
Department of Biochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Israel.
Neurosci Lett. 1991 Apr 29;125(2):231-4. doi: 10.1016/0304-3940(91)90036-s.
The opioid peptide dynorphin A(1-8) (1 micron) increased acetylcholine release from the Torpedo electric organ by approximately twofold. This effect was reversed by the opiate antagonist naloxone. The effect of Dyn A(1-8) on acetylcholine release was found to vary in magnitude with the seasons of the year, with maximal enhancement being observed in the summer and none in winter. Dynorphin B, methionine-enkephalin and leucine-enkephalin also increased acetylcholine release and showed similar seasonal variations. These findings suggest that acetylcholine release from Torpedo electromotor neurons is regulated by opiate receptors. The physiological significance of these observations is discussed in view of the previous findings that the Torpedo neurons contain an endogenous enkephalin-like peptide.
阿片肽强啡肽A(1 - 8)(1微摩尔)可使电鳐电器官的乙酰胆碱释放增加约两倍。这种作用可被阿片拮抗剂纳洛酮逆转。研究发现，强啡肽A(1 - 8)对乙酰胆碱释放的作用大小随一年中的季节变化而不同，夏季观察到最大增强，冬季则无增强。强啡肽B、甲硫氨酸脑啡肽和亮氨酸脑啡肽也可增加乙酰胆碱释放，并表现出类似的季节变化。这些发现表明，电鳐电运动神经元的乙酰胆碱释放受阿片受体调节。鉴于之前的研究发现电鳐神经元含有内源性脑啡肽样肽，本文讨论了这些观察结果的生理学意义。
