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首页> 外文期刊>The European Journal of Neuroscience >Neonatal administration of monosodium glutamate prevents the development of ethanol- but not psychostimulant-induced sensitization: a putative role of the arcuate nucleus.
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Neonatal administration of monosodium glutamate prevents the development of ethanol- but not psychostimulant-induced sensitization: a putative role of the arcuate nucleus.

机译：新生儿服用谷氨酸钠可预防乙醇刺激性疾病的发展，但不能阻止精神兴奋剂诱导的过敏性的发展：弓形核的推定作用。

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摘要

Lesions of the arcuate nucleus by monosodium glutamate, goldthioglucose and oestradiol valerate treatments are known to prevent the acute stimulating effect of ethanol in mice. On the basis of these results, the current study analysed whether a lesion of the arcuate nucleus by monosodium glutamate was able to block ethanol-induced locomotor sensitization. To produce the arcuate nucleus lesions, pups were injected with saline or monosodium glutamate (4 mg/g body weight) subcutaneously on 5 alternate days, starting on postnatal day one. Sensitization treatments began 10 weeks after the initial lesions. Sensitization training consisted of six trials on alternate days, in which groups of mice were treated with ethanol (2 g/kg) or saline, and then tested in an open-field for the induction of locomotor activity. The present study demonstrated that animals with monosodium glutamate-induced lesions did not develop locomotor sensitization to ethanol. Different groups of mice were used to assay blood ethanol levels and to evaluate the effect of arcuate nucleus lesions on psychostimulant-induced locomotor sensitization. Sensitization to cocaine or amphetamine was spared in monosodium glutamate-pre-treated animals, although the lesion of arcuate nucleus reduced the sensitivity of mice to cocaine. Our findings therefore suggest that the arcuate nucleus may be critical for the neuroadaptations that underlie the behavioural sensitization to ethanol, in contrast to those mediating psychostimulant-induced sensitization.
机译：谷氨酸钠，硫代葡萄糖酸金和戊酸雌二醇的处理对弓状核的损害可防止乙醇对小鼠的急性刺激作用。基于这些结果，当前的研究分析了谷氨酸钠对弓形核的损害是否能够阻止乙醇诱导的运动敏化。为了产生弓形的核损伤，从出生后第一天开始，每隔5天皮下给幼犬皮下注射生理盐水或味精（4 mg / g体重）。初始病变后10周开始敏化治疗。敏化训练由隔天进行的六次试验组成，其中每组小鼠均用乙醇（2 g / kg）或生理盐水处理，然后在开阔地带进行运动活性的诱导测试。本研究表明，具有味精诱导的损伤的动物不会对乙醇产生运动敏感性。使用不同组的小鼠分析血液中的乙醇含量，并评估弓形核损伤对精神刺激药引起的运动敏化的影响。谷氨酸钠预处理过的动物对可卡因或苯丙胺的过敏反应没有，尽管弓状核的损伤降低了小鼠对可卡因的敏感性。因此，我们的发现表明，与介导精神兴奋剂诱导的敏化相反，弓形核可能是对乙醇行为敏化的神经适应的关键。

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