Diana M, Pistis M, Muntoni A, Gessa G
Department of Neuroscience B.B. Brodie, University of Cagliari, Italy.
Eur J Pharmacol. 1993 Jan 19;230(3):363-5. doi: 10.1016/0014-2999(93)90574-2.
The effect of intravenous administration of gamma-hydroxybutyric acid (GHB) (50-400 mg/kg) on the firing rate of substantia nigra pars reticulata (SN-PR) neurons was studied by making single cell extracellular recordings in unanesthetized rats. For comparison, the effect of intravenous muscimol (0.5-2 mg/kg) and ethanol (0.5-2 g/kg) was also studied. GHB produced variable effects: dose-related inhibition in 7 out of 18 (38.8%) neurons and no significant change in 11 out of 18 (61.2%) neurons tested. In contrast, muscimol and ethanol produced a dose-related inhibition of the SN-PR firing rate. The results indicate that GHB, unlike muscimol and ethanol, has no profound effect on the activity of SN-PR neurons, and thus disinhibition of dopaminergic units, through inhibition of SN-PR neurons, is probably not the mechanism by which GHB stimulates the firing rate of dopaminergic neurons.
通过对未麻醉大鼠进行单细胞细胞外记录，研究了静脉注射γ-羟基丁酸（GHB）（50 - 400毫克/千克）对黑质网状部（SN-PR）神经元放电频率的影响。作为对照，还研究了静脉注射蝇蕈醇（0.5 - 2毫克/千克）和乙醇（0.5 - 2克/千克）的影响。GHB产生了不同的效应：在18个测试神经元中有7个（38.8%）出现剂量相关的抑制，18个中有11个（61.2%）无显著变化。相比之下，蝇蕈醇和乙醇对SN-PR放电频率产生剂量相关的抑制。结果表明，与蝇蕈醇和乙醇不同，GHB对SN-PR神经元的活动没有深远影响，因此，通过抑制SN-PR神经元来解除对多巴胺能神经元的抑制，可能不是GHB刺激多巴胺能神经元放电频率的机制。
