Wu C
Department of Pharmacology, Gothenburg University, Sweden.
Neurosci Lett. 1994 Apr 25;171(1-2):105-8. doi: 10.1016/0304-3940(94)90616-5.
It was found that systemic application of ethanol induced brain ascorbate (AA) release. In order to study the mechanism of ethanol-evoked AA release, the role of brain glutamatergic neurotransmission was investigated using in vivo voltammetry in the striatum of freely moving rats. Pretreatment with L-trans-pyrrolidine-2,4-dicarboxylate (PDC, 10 nmol, i.c.v.), a glutamate (Glu) uptake blocker, potentiated ethanol (1 g/kg, intraperitoneal injection, i.p.)-evoked release of brain AA. N-methyl-D-aspartate (NMDA, 1 nmol, i.c.v.) produced a fast transient increase in extracellular AA, whereas alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA, 1 nmol, i.c.v.) produced a decrease in extracellular AA (75.8 +/- 3% of control). Kainate (KA, 1 nmol, i.c.v.) produced an initial decrease (48.7 +/- 11.7% of control) then an increase (250 +/- 68.5% of control) in extracellular AA. These results suggest that systemic administration of ethanol may affect the release or uptake of brain glutamatergic neurotransmitters which appear to regulate brain AA release. The NMDA, but not the non-NMDA, type of Glu receptor may be responsible for this regulation.
研究发现，全身应用乙醇可诱导脑内抗坏血酸（AA）释放。为了研究乙醇诱发AA释放的机制，利用体内伏安法在自由活动大鼠的纹状体中研究了脑谷氨酸能神经传递的作用。用L-反式吡咯烷-2,4-二羧酸（PDC，10 nmol，脑室内注射，i.c.v.）预处理，一种谷氨酸（Glu）摄取阻滞剂，可增强乙醇（1 g/kg，腹腔注射，i.p.）诱发的脑AA释放。N-甲基-D-天冬氨酸（NMDA，1 nmol，脑室内注射）使细胞外AA快速短暂增加，而α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA，1 nmol，脑室内注射）使细胞外AA减少（为对照的75.8±3%）。海人藻酸（KA，1 nmol，脑室内注射）使细胞外AA先减少（为对照的48.7±11.7%），然后增加（为对照的250±68.5%）。这些结果表明，全身给予乙醇可能影响脑谷氨酸能神经递质的释放或摄取，而这些神经递质似乎调节脑AA释放。谷氨酸受体的NMDA型而非非NMDA型可能负责这种调节。
