Svensson L, Wu C, Johannessen K, Engel J A
Department of Pharmacology, University of Göteborg, Sweden.
Alcohol. 1992 Nov-Dec;9(6):535-40. doi: 10.1016/0741-8329(92)90093-p.
An in vivo voltammetry technique was used to monitor the extracellular ascorbate (AA) concentration in the nucleus accumbens and striatum of unanesthetized, freely moving rats. A single injection of ethanol, 1.0 g/kg intraperitoneally (IP), induced a significant increase in extracellular AA concentration in both the nucleus accumbens and striatum. This effect was dose dependent within a dose range from 0.5-2.0 g/kg. 4-Methylpyrazole (50 mg/kg, IP), which inhibits alcoholdehydrogenase, could not prevent the increase in AA concentration, evoked by ethanol. Furthermore, systemic administration of acetaldehyde (20 mg/kg, IP), the main metabolite of ethanol, did not have any effect on the level of AA in the nucleus accumbens or striatum. These results show that ethanol can alter the brain extracellular AA levels and that this effect seems to be attributed to ethanol itself and not to acetaldehyde. Consequently, these results indicate that a role for AA in the action of ethanol in the brain should be considered.
采用体内伏安法技术监测未麻醉、自由活动大鼠伏隔核和纹状体细胞外抗坏血酸（AA）浓度。腹腔注射1.0 g/kg乙醇可使伏隔核和纹状体细胞外AA浓度显著升高。在0.5 - 2.0 g/kg剂量范围内，该效应呈剂量依赖性。抑制乙醇脱氢酶的4 - 甲基吡唑（50 mg/kg，腹腔注射）不能阻止乙醇引起的AA浓度升高。此外，乙醇的主要代谢产物乙醛（20 mg/kg，腹腔注射）全身给药对伏隔核或纹状体中AA水平没有任何影响。这些结果表明，乙醇可改变脑内细胞外AA水平，且这种效应似乎归因于乙醇本身而非乙醛。因此，这些结果表明应考虑AA在乙醇对脑作用中的作用。
