Deletion of N-type calcium channels alters ethanol reward and reduces ethanol consumption in mice.
N-type calcium channels are modulated by acute and chronic ethanol exposure in vitro at concentrations known to affect humans, but it is not known whether N-type channels are important for behavioral responses to ethanol in vivo. Here, we show that in mice lacking functional N-type calcium channels, voluntary ethanol consumption is reduced and place preference is developed only at a low dose of ethanol. The hypnotic effects of ethanol are also substantially diminished, whereas ethanol-induced ataxia is mildly increased. These results demonstrate that N-type calcium channels modulate acute responses to ethanol and are important mediators of ethanol reward and preference.
Newton
Philip M
PM
Ernest Gallo Clinic and Research Center, Department of Neurology, University of California, San Francisco, Emeryville, California 94608, USA.
Orr
Christine J
CJ
Wallace
Melisa J
MJ
Kim
Chanki
C
Shin
Hee-Sup
HS
Messing
Robert O
RO
D000428:Alcohol Drinking / Q000503:physiopathology*; D000818:Animals; D001362:Avoidance Learning / Q000502:physiology; D020864:Calcium Channels, N-Type / Q000235:genetics / Q000502:physiology*; D003213:Conditioning, Psychological / Q000502:physiology; D000431:Ethanol / Q000494:pharmacology*; D006993:Hypnotics and Sedatives / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D004856:Postural Balance / Q000187:drug effects / Q000502:physiology; D012201:Reward
C500963:Cacna1b protein, mouse; D020864:Calcium Channels, N-Type; D006993:Hypnotics and Sedatives; D000431:Ethanol