Mereu G, Gessa G L
Brain Res. 1985 Dec 23;360(1-2):325-30. doi: 10.1016/0006-8993(85)91249-1.
The intravenous administration of relatively low doses of ethanol (0.25-2.00 g/kg) produced a dose-dependent inhibition of the firing rate of the neurons located in the substantia nigra, pars reticulata (PR neurons). This effect was eliminated both by picrotoxin and bicuculline, two blockers of gamma-aminobutyric acid (GABA) transmission, and potentiated by muscimol (a direct GABA agonist) and diazepam (a representative of the benzodiazepine class which facilitate GABA transmission). The specific benzodiazepine antagonist, Ro 15-1788, blocked the potentiating effect of diazepam on the ethanol effect but failed to antagonize ethanol-induced inhibition of the firing rate of the neurons. These results indicate that ethanol might inhibit the firing of PR neurons through a GABAergic mechanism. Moreover, since PR neurons are thought to exert an inhibitory control on nigral dopaminergic neurons, it is suggested that the depression of the activity of such inhibitory interneurons may be responsible for ethanol-induced stimulation of dopaminergic activity.
静脉注射相对低剂量的乙醇（0.25 - 2.00克/千克）会对位于黑质网状部的神经元（PR神经元）的放电频率产生剂量依赖性抑制。这种效应可被印防己毒素和荷包牡丹碱消除，这两种药物是γ-氨基丁酸（GABA）传递的阻断剂，而可被蝇蕈醇（一种直接的GABA激动剂）和地西泮（促进GABA传递的苯二氮䓬类代表药物）增强。特异性苯二氮䓬拮抗剂Ro 15 - 1788可阻断地西泮对乙醇效应的增强作用，但无法拮抗乙醇诱导的神经元放电频率抑制。这些结果表明，乙醇可能通过GABA能机制抑制PR神经元的放电。此外，由于PR神经元被认为对黑质多巴胺能神经元发挥抑制性控制作用，因此有人提出，此类抑制性中间神经元活性的降低可能是乙醇诱导多巴胺能活性刺激的原因。
