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.
| Original language | English |
|---|---|
| Pages (from-to) | 493-9 |
| Number of pages | 7 |
| Journal | Genes, Brain, and Behavior |
| Volume | 8 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - Jul 2009 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Alcohol-Induced Disorders, Nervous System
- Alcoholism
- Amygdala
- Animals
- Brain Chemistry
- Central Nervous System Depressants
- Conditioning (Psychology)
- Disease Models, Animal
- Ethanol
- Gene Frequency
- Genetic Predisposition to Disease
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Protein Kinase C-epsilon
- Reward
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