Lendvai B, Sándor N T, Sándor A
Department of Pharmacology, Hungarian Academy of Sciencies, Budapest.
Acta Physiol Hung. 1993;81(1):19-28.
In the present study the effect of selective opiate antagonists on the release of acetylcholine (ACh) and dopamine (DA) was studied in striatal slices. beta-funaltrexamine (beta-FNA) a mu receptor antagonist, naltrindole (NTI) a delta receptor antagonist and a kappa receptor antagonist nor-binaltorphimine (nor-BNI) were used to selectively block the different opioid receptor subpopulations located on the axon terminals. The receptor activation was examined on superfused slices from rat striatum previously labelled with [3H]choline or [3H]dopamine. We found that both beta-FNA and NTI significantly enhanced the evoked release of ACh using electrical field stimulation but it occurred only in those cases when dopaminergic input was impaired either by lesion of the nigrostriatal tract or by D2 dopamine receptor blocade. By contrast, under these conditions the opiate antagonists had no modulatory effect on the release of DA. Our data suggest that the release of ACh in the striatum is under the tonic control of endogenous opioid peptides. This effect is mediated via mu and delta opioid receptors. However the striatal DA release does not seem to be controlled tonically by opioid peptides.
在本研究中，我们在纹状体切片中研究了选择性阿片拮抗剂对乙酰胆碱（ACh）和多巴胺（DA）释放的影响。使用μ受体拮抗剂β-氟纳曲明（β-FNA）、δ受体拮抗剂纳曲吲哚（NTI）和κ受体拮抗剂诺宾那托啡（nor-BNI）选择性阻断位于轴突终末的不同阿片受体亚群。在预先用[3H]胆碱或[3H]多巴胺标记的大鼠纹状体灌流切片上检测受体激活情况。我们发现，β-FNA和NTI均能通过电场刺激显著增强诱发的ACh释放，但仅在黑质纹状体通路损伤或D2多巴胺受体阻断导致多巴胺能输入受损的情况下才会发生。相比之下，在这些条件下，阿片拮抗剂对DA的释放没有调节作用。我们的数据表明，纹状体中ACh的释放受内源性阿片肽的紧张性控制。这种作用是通过μ和δ阿片受体介导的。然而，纹状体DA释放似乎不受阿片肽的紧张性控制。
