Reinterpretation of the literature indicates differential sensitivities of long-sleep and short-sleep mice are not specific to alcohol.

This paper reviews the findings and conclusions of the literature pertinent to the Long-Sleep and Short-Sleep selectively-bred lines of mice and challenges the widely-held notion that the selective breeding program was successful in separating alleles for specific sensitivities to just alcohol. Rather, it is argued that these lines of mice were selected for differing activity of a more general process. Recent evidence, as well as reevaluated previous evidence, indicates that Long-Sleep mice are more sensitive to the soporific effects of three major classes of CNS depressants (alcohols, barbiturates, and benzodiazepines), as well as many other anesthesia-inducing compounds (adenosine, chloral hydrate, trichloroethanol, paraldehyde, nitrous oxide, enflurane, and isoflurane). Further, much evidence also supports the conclusion that most of these hypnotic-depressants and anesthetics could exert their soporific influence by a potentiation of GABA activity. The other characteristic of interest in this regard is susceptibility to convulsions. Short-Sleep mice have significantly lower thresholds to both flurothyl-induced and bicuculline-induced convulsions, as well as being more likely to suffer from paroxysms during ethanol withdrawal.