Hybrid mice produced by crossing CBA and C57BL lines were deprived of
alcohol for three days after prolonged prior access. Subsequently, whe
n access was first given to a flavored 30% alcohol solution, about hal
f of the mice showed a greatly elevated rate of drinking during the fi
rst 1.5 h, characteristic of the alcohol-deprivation effect (ADE), but
other mice showed no increase. Repeating the test three weeks later s
howed 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 applica
tion of L-glutamate to the frontal cortex prevented the subsequent ele
vation of alcohol drinking during the first 1.5 h after deprivation bu
t did not alter drinking during the remaining 22.5 h. L-glutamate trea
tment 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 hyb
rid mice having and lacking an ADE might be used for determining the n
euronal mechanisms responsible for the effect.