Boyadjieva N I, Sarkar D K
Department of Veterinary and Comparative Anatomy. Pharmacology and Physiology, Washington State University, Pullman 99164-6520, USA.
J Neuroendocrinol. 1995 Nov;7(11):819-25. doi: 10.1111/j.1365-2826.1995.tb00720.x.
In the present study, we determined the effects of dopamine receptor agonists and antagonists on basal and ethanol-modulated beta-endorphin (beta-EP) secretion from hypothalamic neurons in primary cultures. Treatment with various concentrations of dopamine D1 agonist SKF 38393 and D1 antagonist SCH 23390 did not affect basal IR-beta-EP release. However, dopamine D2 receptor agonist LY 141865 reduced basal immunoreactive (IR)-beta-EP release in a concentration dependent manner. D2 receptor antagonist, sulpiride, on the other hand, stimulated basal IR-beta-EP release and blocked LY 141865-induced inhibition of IR-beta-EP release in a concentration dependent manner. When the actions of these DA receptor agents on ethanol-modulated IR-beta-EP release were studied, both D1 and D2 receptor agents failed to affect ethanol-modulated IR-beta-EP release. These data suggest that the endogenous secretion of beta-EP from hypothalamic neurons is under the influence of an inhibitory dopaminergic system involving the D2 receptor. Furthermore, ethanol's effects on beta-EP secretion are not mediated by dopamine.
在本研究中，我们测定了多巴胺受体激动剂和拮抗剂对原代培养的下丘脑神经元基础及乙醇调节的β-内啡肽（β-EP）分泌的影响。用不同浓度的多巴胺D1激动剂SKF 38393和D1拮抗剂SCH 23390处理，不影响基础免疫反应性β-EP的释放。然而，多巴胺D2受体激动剂LY 141865以浓度依赖的方式降低基础免疫反应性（IR）-β-EP的释放。另一方面，D2受体拮抗剂舒必利以浓度依赖的方式刺激基础IR-β-EP的释放，并阻断LY 141865诱导的IR-β-EP释放的抑制作用。当研究这些多巴胺受体药物对乙醇调节的IR-β-EP释放的作用时，D1和D2受体药物均未能影响乙醇调节的IR-β-EP释放。这些数据表明，下丘脑神经元β-EP的内源性分泌受涉及D2受体的抑制性多巴胺能系统的影响。此外，乙醇对β-EP分泌的影响不是由多巴胺介导的。
