Open AccessAmygdala protein kinase C epsilon controls alcohol consumption
Author(s) -
Lesscher H. M. B.,
Wallace M. J.,
Zeng L.,
Wang V.,
Deitchman J. K.,
McMahon T.,
Messing R. O.,
Newton P. M.
Publication year - 2009
Publication title -
genes, brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.315
H-Index - 91
eISSN - 1601-183X
pISSN - 1601-1848
DOI - 10.1111/j.1601-183x.2009.00485.x
Subject(s) - amygdala , protein kinase a , ethanol , gene knockdown , endocrinology , medicine , wild type , alcohol consumption , consumption (sociology) , biology , kinase , chemistry , alcohol , microbiology and biotechnology , biochemistry , gene , social science , sociology , mutant
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.