Ruzicka B B, Jhamandas K
Department of Pharmacology and Toxicology, Queen's University, Kingston, Ont., Canada.
Can J Physiol Pharmacol. 1991 Mar;69(3):414-8. doi: 10.1139/y91-063.
Previous investigations have shown that the activation of delta-opioid receptors depresses the release of acetylcholine (ACh) in the rat caudate putamen. This finding raised the possibility that the release of ACh is similarly modulated in the globus pallidus, a region containing a distinct population of cholinergic neurons and enriched in enkephalinergic nerve terminals. In the present study the pallidal release of ACh was characterized and the effects of delta-opioid receptor activation on this release were examined. The results show that this release is stimulated by high K+ in a concentration- and Ca(2+)-dependent manner. D-Pen2,L-Pen5-enkephalin (0.1-10 microM), a selective delta-opioid receptor agonist, produced a dose-related inhibition of the 25 mM K(+)-evoked tritium release. The maximal inhibitory effect, representing a 34% decrease in the K(+)-induced tritium release, was observed at a concentration of 1 microM. This opioid effect was attenuated by the selective delta-opioid receptor antagonist, ICI 174864 (1 microM). These findings support the role of a delta-opioid receptor in the modulation of ACh release in the rat globus pallidus.
先前的研究表明,δ-阿片受体的激活会抑制大鼠尾状核壳核中乙酰胆碱(ACh)的释放。这一发现引发了一种可能性,即苍白球中ACh的释放也受到类似的调节,苍白球是一个含有独特胆碱能神经元群体且脑啡肽能神经末梢丰富的区域。在本研究中,对苍白球中ACh的释放进行了表征,并研究了δ-阿片受体激活对该释放的影响。结果表明,这种释放受到高钾离子以浓度和钙离子依赖的方式刺激。D-青霉胺2,L-青霉胺5-脑啡肽(0.1-10微摩尔),一种选择性δ-阿片受体激动剂,对25毫摩尔钾离子诱发的氚释放产生剂量相关的抑制作用。在1微摩尔浓度下观察到最大抑制作用,代表钾离子诱导的氚释放减少34%。这种阿片样物质效应被选择性δ-阿片受体拮抗剂ICI 174864(1微摩尔)减弱。这些发现支持了δ-阿片受体在调节大鼠苍白球中ACh释放中的作用。