L-glutamate abolishes differential responses to alcohol deprivation in mice.
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.
Salimov
R M
RM
Institute of Pharmacology, Russian Academy of Medical Sciences, Moscow.
Salimova
N B
NB
D000428:Alcohol Drinking; D000437:Alcoholism / Q000503:physiopathology; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D000431:Ethanol / Q000008:administration & dosage*; D005106:Exploratory Behavior / Q000187:drug effects; D005625:Frontal Lobe / Q000187:drug effects; D005971:Glutamates / Q000008:administration & dosage / Q000494:pharmacology*; D018698:Glutamic Acid; D006824:Hybridization, Genetic; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA
D005971:Glutamates; D000431:Ethanol; D018698:Glutamic Acid