Note: Outstanding Young Investigators Awardee, 9th Annual Meeting of the International Behavioural and Neural Genetics Society,Doorwerth, The Netherlands, May 21–25, 2007.
Amygdala protein kinase C epsilon controls alcohol consumption
Version of Record online: 19 FEB 2009
© 2009 The Authors Journal compilation © 2009 Blackwell Publishing Ltd/International Behavioural and Neural Genetics Society
Genes, Brain and Behavior
Volume 8, Issue 5, pages 493–499, July 2009
How to Cite
Lesscher, H. M. B., Wallace, M. J., Zeng, L., Wang, V., Deitchman, J. K., McMahon, T., Messing, R. O. and Newton, P. M. (2009), Amygdala protein kinase C epsilon controls alcohol consumption. Genes, Brain and Behavior, 8: 493–499. doi: 10.1111/j.1601-183X.2009.00485.x
Present address: Rudolf Magnus Institute of Neuroscience, Department of Neuroscience and Pharmacology, University Medical Center Utrecht, 3584 CG Utrecht, The Netherlands
- Issue online: 15 JUL 2009
- Version of Record online: 19 FEB 2009
- Received 8 August 2008, revised 11 January 2009, accepted for publication 19 January 2009
- limited access paradigm;
- RNA interference;
- protein kinase C epsilon;
Alcoholism is a progressive disorder that involves the amygdala. Mice lacking protein kinase C epsilon (PKCɛ) show reduced ethanol consumption, sensitivity and reward. We therefore investigated whether PKCɛ signaling in the amygdala is involved in ethanol consumption. Local knockdown of PKCɛ in the amygdala reduced ethanol consumption and preference in a limited-access paradigm. Further, mice that are heterozygous for the PKCɛ allele consume less ethanol compared with wild-type mice in this paradigm. These mice have a >50% reduction in the abundance of PKCɛ in the amygdala compared with wild-type mice. We conclude that amygdala PKCɛ is important for ethanol consumption in mice.