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- W2014134436 abstract "Hybrid mice produced by crossing CBA and C57BL lines were deprived of alcohol for three days after prolonged prior access. Subsequently, when access was first given to a flavored 30% alcohol solution, about half of the mice showed a greatly elevated rate of drinking during the first 1.5 h, characteristic of the alcohol-deprivation effect (ADE), but other mice showed no increase. Repeating the test three weeks later showed that having or lacking an ADE is a stable group characteristic. Behavioral differences were found on cross-maze and slip funnel tests between mice that had an ADE and those that lacked it. Topical application of L-glutamate to the frontal cortex prevented the subsequent elevation of alcohol drinking during the first 1.5 h after deprivation but did not alter drinking during the remaining 22.5 h. L-glutamate treatment also affected those cross-maze behaviors found to be related to the ADE. The results suggest that frontal cortex neurons sensitive to L-glutamate are necessary for the ADE and that comparisons between hybrid mice having and lacking an ADE might be used for determining the neuronal mechanisms responsible for the effect." @default.
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- W2014134436 title "L-glutamate abolishes differential responses to alcohol deprivation in mice" @default.
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- W2014134436 doi "https://doi.org/10.1016/0741-8329(93)90001-5" @default.
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