Sandor N T, Lendvai B, Vizi E S
Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest.
Brain Res Bull. 1992 Sep-Oct;29(3-4):369-73. doi: 10.1016/0361-9230(92)90070-e.
We investigated the effect of selective opiate antagonists on striatal acetylcholine (ACh) and dopamine (DA) release. The mu-receptor antagonist beta-funaltrexamine (beta-FNA), the delta-antagonist naltrindole (NTI), and the kappa-antagonist norbinaltorphimine (nor-BNI) were used to selectively block different subtypes of opiate receptors. The experiments were carried out on isolated superfused striatal slices of rats, loaded with [3H]choline or [3H]dopamine. beta-FNA and NTI significantly enhanced the electrical field stimulation-evoked release of ACh but only if the dopaminergic input had been impaired either by chemical denervation or D2 dopamine receptor blockade. By contrast, neither the selective nor nonselective antagonists had any modulatory effect on the release of dopamine. It is concluded, therefore, that the release of ACh is tonically controlled by endogenous opioid peptide(s) through the stimulation of mu- and delta-opiate receptors located on cholinergic axon terminals, in addition to the tonic control by DA.
我们研究了选择性阿片拮抗剂对纹状体乙酰胆碱（ACh）和多巴胺（DA）释放的影响。使用μ受体拮抗剂β-芬太尼酰（β-FNA）、δ拮抗剂纳曲吲哚（NTI）和κ拮抗剂 norbinaltorphimine（nor-BNI）来选择性阻断不同亚型的阿片受体。实验在加载了[3H]胆碱或[3H]多巴胺的大鼠离体灌流纹状体切片上进行。β-FNA 和 NTI 显著增强了电场刺激诱发的 ACh 释放，但前提是多巴胺能输入已通过化学去神经支配或 D2 多巴胺受体阻断受损。相比之下，选择性和非选择性拮抗剂对多巴胺释放均无任何调节作用。因此得出结论，除了 DA 的紧张性控制外，ACh 的释放还受到内源性阿片肽通过刺激位于胆碱能轴突终末的μ和δ阿片受体的紧张性控制。
