Ethanol self-administration in long sleep and short sleep mice indicates reinforcement is not inversely related to neurosensitivity.

Studies of ethanol drinking suggest an inverse correlation between innate sensitivity to ethanol and behavior reinforced by this drug. The present study investigated ethanol reinforced behavior in mice selectively bred for high, Long Sleep/Institute for Behavioral Genetics (LS), and low, Short Sleep/Institute for Behavioral Genetics (SS), sensitivity to ethanol. Results show that both lines will drink large amounts of ethanol postprandially. However, in the absence of food presentation, LS and SS mice differed significantly in ethanol reinforced behavior. Ethanol maintained higher rates of responding, greater intake and higher blood ethanol levels in LS relative to SS mice across increasing fixed-ratio values. Ethanol did not maintain fixed-ratio lever pressing above rates maintained by vehicle in SS mice. Responding for and consumption of 8% ethanol significantly exceeded that of vehicle only in LS mice. Response rates of LS mice showed a typical inverted U-shaped relationship to ethanol concentration. Postsession blood ethanol levels and body temperatures indicated pharmacologically significant ethanol intake only in LS mice. Thus, ethanol served as an effective reinforcer in LS mice across a range of environmental conditions. Conversely, ethanol was not established as a positive reinforcer in SS mice under any of the broad range of conditions studied. These results are not consistent with the frequently reported negative correlation between ethanol intake and sensitivity to ethanol and rule out a causal basis for correlations seen between these traits.