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.2009 Jul;8(5):493-9.
doi: 10.1111/j.1601-183X.2009.00485.x. Epub 2009 Feb 19.

Amygdala protein kinase C epsilon controls alcohol consumption

Affiliations

Amygdala protein kinase C epsilon controls alcohol consumption

H M B Lesscher et al. Genes Brain Behav.2009 Jul.

Abstract

Alcoholism is a progressive disorder that involves the amygdala. Mice lacking protein kinase C epsilon (PKCepsilon) show reduced ethanol consumption, sensitivity and reward. We therefore investigated whether PKCepsilon signaling in the amygdala is involved in ethanol consumption. Local knockdown of PKCepsilon in the amygdala reduced ethanol consumption and preference in a limited-access paradigm. Further, mice that are heterozygous for the PKCepsilon allele consume less ethanol compared with wild-type mice in this paradigm. These mice have a >50% reduction in the abundance of PKCepsilon in the amygdala compared with wild-type mice. We conclude that amygdala PKCepsilon is important for ethanol consumption in mice.

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Figures

Figure 1
Figure 1. High levels of ethanol consumption under conditions of limited access are naltrexone-sensitive
Shown are mean ± S.E.M. values from 9 male, wild type mice. Ethanol intake (A), ethanol preference (B) and total fluid intake (C) increased over the 10-day period. Mice were allowed to drink for an additional 4 days. Injection of naltrexone (NTX, 1 mg/kg)i.p. immediately prior to the 2-h session on day 14 reduced ethanol intake (D) and preference (E) without affecting total fluid intake (F). *P < 0.05 compared with vehicle treatment on day 13, by one-tailed, pairedt-test.
Figure 2
Figure 2. Local knockdown of PKCε in the amygdala reduces ethanol intake under limited gaccess conditions
Over 4 consecutive weeks of daily ethanol consumption under conditions of daily limited access, mice treated with control shRNA (n = 9) increased their ethanol intake(A) and ethanol preference(B), whereas mice treated with the 1845 PKCε shRNA (n = 9) did not.(C) Total fluid intake increased over 4 weeks similarly in both treatment groups. Control and PKCε shRNA treated mice consumed equal amounts of 20% sucrose (D) and 0.03 mM quinine (E) in 2-h sessions. *P < 0.05 compared with 1845 PKCε shRNA-treated mice bypost-hoc Bonferroni test for intake in week 3 (t16 = 4.2,P < 0.001) and week 4 (t16 = 3.5,P < 0.01) and for preference in week 3 (t16 = 3.1,P < 0.01) and week 4 (t16 = 2.6,P < 0.05).
Figure 3
Figure 3. Reduced abundance of PKC ε in the amygdala of PKCε+/−mice.
Abundance of PKC ε was determined by quantitative western blot analysis. Values are expressed as a percentage of the mean abundance in wild type whole brain (A) (n=3 for both genotypes) and amygdala (B) (n=4 for both genotypes). A representative blot for amygdala samples is also shown (C). *P < 0.05 compared to wild type mice for whole brain (t4 = 5.3,P < 0.01) and amygdala (t6 = 4.5,P < 0.01).
Figure 4
Figure 4
PKCε+/−mice show reduced ethanol intake under limited access conditions. Over 4 consecutive weeks of daily ethanol consumption under conditions of limited access, PKCε+/− mice (n = 11) showed reduced ethanol intake(A) and preference(B), compared with wild-type mice (n=12), with no difference in total volume consumed(C) or water consumed(D).
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References

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