Accumbens neurochemical adaptations produced by binge-like alcohol consumption.
Accumbens neurochemical adaptations produced by binge-like alcohol consumption.
复制标题
暴饮暴食引起的伏隔神经化学适应。
DOI：
10.1007/s00213-006-0641-7
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发表时间：
2007
影响因子：
3.4
通讯作者：
Bowers,MScott
中科院分区：
文献类型：
--
作者：
Szumlinski,KarenK;Diab,MahdiE;Friedman,Raquel;Henze,LiezlM;Lominac,KevinD;Bowers,MScott
预定的高酒精消费（SHAC）狂欢饮酒模型是一个简单的，目的：利用SHAC模型，研究酒精对大鼠小脑延髓核（NAC）单胺和氨基酸的影响，探讨酒精中毒的神经生物学基础。小鼠在饮用水、第一次饮用5%酒精（v/v）溶液（SHAC 1）或第六次饮用5%酒精溶液（SHAC 6）期间。第二组的微透析实验评估的神经递质响应酒精挑战注射（1.5或2克/公斤，IP）。ResultsIn两个饮用实验，SHAC 1和SHAC 6小鼠消耗相当数量的酒精在40分钟期间的酒精可用性（~1.5克/公斤）和总液体摄入量是相似的水和SHAC 1/6小鼠之间。尽管在酒精消耗的相似性，酒精介导的GABA和血清素的细胞外浓度的增加减少，但谷氨酸增加的NAC的SHAC 6小鼠，相对于SHAC 1动物。SHAC 1和SHAC 6小鼠在饮酒期间细胞外多巴胺没有观察到差异。在酒精注射后，SHAC 6小鼠也表现出致敏的谷氨酸释放，但与水或SHAC 1动物的任何其他神经递质检查没有差异。脑酒精浓度并没有显着差异组注射后。ConclusionsRepeated回合的高酒精消费诱导NAC内的抑制性和兴奋性神经传递之间的不平衡，可能会驱动过度饮酒行为。
RationaleThe Scheduled High Alcohol Consumption (SHAC) binge drinking model is a simple, partial murine model with which to investigate some of the neurobiological underpinnings of alcoholism.ObjectivesThe SHAC model was used to characterize monoamine and amino acid adaptations produced in the nucleus accumbens (NAC) by repeated bouts of high alcohol consumption.MethodsIn vivo microdialysis was conducted in the NAC of C57BL/6J (B6) mice during consumption of water, a 5% alcohol (v/v) solution for the first time (SHAC1) or a 5% alcohol solution for the sixth time (SHAC6). A second set of microdialysis experiments assessed the neurotransmitter response to an alcohol challenge injection (1.5 or 2 g/kg, IP).ResultsIn both drinking experiments, SHAC1 and SHAC6 mice consumed comparable amounts of alcohol during the 40-min period of alcohol availability (~1.5 g/kg) and total fluid intake was similar between water and SHAC1/6 mice. Despite the similarity in alcohol consumption, alcohol-mediated increases in the extracellular concentration of GABA and serotonin were reduced, but glutamate was increased in the NAC of SHAC6 mice, relative to SHAC1 animals. No differences were observed in extracellular dopamine between SHAC1 and SHAC6 mice during alcohol consumption. After alcohol injection, SHAC6 mice also exhibited sensitized glutamate release, but did not differ from water or SHAC1 animals for any of the other neurotransmitters examined. Brain alcohol concentrations did not differ between groups after injection.ConclusionsRepeated bouts of high alcohol consumption induce an imbalance between inhibitory and excitatory neurotransmission within the NAC that may drive excessive drinking behavior.