EFFECT OF OPIOIDS ON ACETYLCHOLINE-RELEASE EVOKED BY K+ OR GLUTAMIC-ACID FROM RAT NEOSTRIATAL SLICES
EFFECT OF OPIOIDS ON ACETYLCHOLINE-RELEASE EVOKED BY K+ OR GLUTAMIC-ACID FROM RAT NEOSTRIATAL SLICES
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DOI：
10.1016/0006-8993(90)91633-r
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发表时间：
1990-07-16
期刊：
影响因子：
2.9
通讯作者：
MARSAL, J
中科院分区：
文献类型：
--
作者：
ARENAS, E;ALBERCH, J;MARSAL, J
通过化学发光法测量大鼠纹状体切片的内源性乙酰胆碱（ACh）释放。测试了几种阿片类药物调节钾离子 (K+) 或谷氨酸 (GLU) 引起的乙酰胆碱释放的能力。吗啡、[D-Ala2、Gly(ol)5]-脑啡肽 (DAGO)、[D-Ala2,D-Leu5]-脑啡肽 (DADLE) 和 [D-Pen2-D-Pen5]-脑啡肽 (DPDPE) 被发现对 K+- 或 GLU 诱发的 ACh 释放具有抑制作用。这种作用被纳洛酮完全阻断，但这种拮抗剂本身对乙酰胆碱释放没有影响。 μ-阿片激动剂（吗啡和DAGO）对K+引起的ACh释放的作用对河豚毒素（TTX）敏感，但δ-阿片激动剂（DADLE和DPDPE）不敏感。 GLU 引发的释放在 TTX 存在的情况下被废除。强啡肽-(1-13)对κ-阿片受体的激活对K+-或GLU-诱发的ACh释放没有影响。结论是μ-和δ-鸦片激动剂，而非κ，对纹状体胆碱能中间神经元施加抑制控制，但具有不同的作用机制或受体定位。皮质纹状体谷氨酸能神经元在乙酰胆碱-阿片类药物系统的相互作用中发挥重要作用。
Endogenous acetylcholine (ACh) release from rat striatal slices was measured by a chemiluminescent method. Several opiate agents were tested for their ability to modulate ACh release evoked by potassium ions (K+) or glutamic acid (GLU). Morphine, [D-Ala2, Gly(ol)5]-enkephalin (DAGO), [D-Ala2,D-Leu5]-enkephalin (DADLE) and [D-Pen2-D-Pen5]-enkephalin (DPDPE) were found to have an inhibitory effect on K+- or GLU-evoked ACh release. This effect was completely blocked by naloxone, but this antagonist by itself had no effect on ACh release. The action of .mu.-opiate agonists (morphine and DAGO) on ACh release evoked by K+ was sensitive to tetrodotoxin (TTX), but that of .delta.-opiate agonists (DADLE and DPDPE) was insensitive. The release evoked by GLU was abolished in the presence of TTX. The activation of .kappa.-opiate receptor by dynorphin-(1-13) had no effect on K+- or GLU-evoked ACh release. It is concluded that .mu.- and .delta.-opiate agonists, but not .kappa., exert an inhibitory control on striatal cholinergic interneurons, but with a different mechanism of action or localization of the receptors. Corticostriatal glutamatergic neurons have an important role in the interaction of the ACh-opioid systems.