Hunt W A, Rabin B M, Lee J
Alcohol. 1987 May-Jun;4(3):169-73. doi: 10.1016/0741-8329(87)90039-5.
Two experiments were run to evaluate the role of acetaldehyde and the area postrema in the acquisition of an ethanol-induced conditioned taste aversion. An ethanol-induced taste aversion was observed in male Sprague-Dawley rats with a dose of 4 g/kg. PO, but not after doses of 1 or 2 g/kg. Pretreatment with 4-methylpyrazole (8 mg/kg, IP), which itself did not induce an aversion as compared to pyrazole (68 mg/kg, IP) that did, and/or prior application of lesions of the area postrema had no influence on the development of an ethanol-induced taste aversion. The results indicate that ethanol-induced taste aversion learning does not result from the metabolism of ethanol to acetaldehyde and does not, like other toxins, involve the mediation of the area postrema.
进行了两项实验以评估乙醛和最后区在乙醇诱导的条件性味觉厌恶习得中的作用。在雄性斯普拉格-道利大鼠中,观察到剂量为4 g/kg经口给予乙醇会诱导味觉厌恶,但剂量为1或2 g/kg时则不会。与能诱导厌恶的吡唑(68 mg/kg,腹腔注射)相比,4-甲基吡唑(8 mg/kg,腹腔注射)本身不会诱导厌恶,对最后区进行损伤预处理和/或预先应用最后区损伤对乙醇诱导的味觉厌恶的发展没有影响。结果表明,乙醇诱导的味觉厌恶学习并非由乙醇代谢为乙醛所致,并且与其他毒素不同,不涉及最后区的介导作用。