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下丘脑-垂体-肾上腺皮质轴在应激后大鼠乙醇摄入中的作用。

The role of the hypothalamic-pituitary-adrenocortical axis in post-stress induced ethanol consumption by rats.

作者信息

Nash J F, Maickel R P

机构信息

Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, IN.

出版信息

Prog Neuropsychopharmacol Biol Psychiatry. 1988;12(5):653-71. doi: 10.1016/0278-5846(88)90010-3.

DOI:10.1016/0278-5846(88)90010-3
PMID:2851859
Abstract
  1. Previous studies conducted in our laboratory demonstrated that rats given a choice between a 0.1% saccharin solution or 10% ethanol/0.1% saccharin solution and repeatedly exposed on an unpredictable basis to stressful stimuli, consumed increasing quantities of the ethanol solution following cessation of stressor presentation as compared to nonstressed control rats. 2. Stressful stimuli potently activate the hypothalamic-pituitary-adrenocortical (HPA) axis, thus a systematic investigation of the HPA axis and its involvement in post-stress induced ethanol consummatory behavior was undertaken. 3. Exposure to repetitive unpredictable stressful stimuli did not induce the free-choice consumption of ethanol in either hypophysectomized rats or chronic dexamethasone treated rats. 4. Adrenalectomized rats exposed to chronic unpredictable stressful stimuli consumed increased quantities of ethanol following cessation of stressful stimuli in both a quantitative and qualitative manner which mirrored that of intact animals. 5. Repeated intravenous administration of exogenous adrenocorticotropin (ACTH1-39) on an unpredictable basis also induced ethanol consuming behavior, following the discontinuation of its administration. 6. These results suggest that elimination of the pituitary or pharmacological antagonism of stress-induced HPA activation will prevent post-stress induced ethanol consummatory behavior. 7. Conversely, activation of a functional hypothalamic-pituitary system or repeated administration of exogenous ACTH1-39 will initiate ethanol consumption in rats. 8. Thus, hormones secreted from the pituitary, namely ACTH, appear to play a crucial role in the post-stress induced initiation of ethanol consuming behavior in rats.
摘要
  1. 我们实验室之前进行的研究表明,在0.1%糖精溶液或10%乙醇/0.1%糖精溶液之间做出选择,并反复在不可预测的基础上暴露于应激刺激的大鼠,与未受应激的对照大鼠相比,在应激源呈现停止后,乙醇溶液的消耗量增加。2. 应激刺激有力地激活下丘脑-垂体-肾上腺皮质(HPA)轴,因此对HPA轴及其在应激后诱导的乙醇消费行为中的作用进行了系统研究。3. 暴露于重复性不可预测应激刺激的大鼠,无论是垂体切除的大鼠还是接受慢性地塞米松治疗的大鼠,都没有出现乙醇的自由选择消费。4. 暴露于慢性不可预测应激刺激的肾上腺切除大鼠,在应激刺激停止后,以定量和定性的方式消耗了更多的乙醇,这与完整动物的情况相似。5. 在不可预测的基础上反复静脉注射外源性促肾上腺皮质激素(ACTH1-39),在停止注射后也诱导了乙醇消费行为。6. 这些结果表明,消除垂体或对应激诱导的HPA激活进行药理学拮抗将预防应激后诱导的乙醇消费行为。7. 相反,功能性下丘脑-垂体系统的激活或反复注射外源性ACTH1-39将引发大鼠的乙醇消费。8. 因此,垂体分泌的激素,即促肾上腺皮质激素,似乎在大鼠应激后诱导的乙醇消费行为的启动中起关键作用。

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