Loss of RAB‐3/A in Caenorhabditis elegans and the mouse affects behavioral response to ethanol

The mechanisms by which ethanol induces changes in behavior are not well understood. Here, we show that Caenorhabditis elegans loss‐of‐function mutations in the synaptic vesicle‐associated RAB‐3 protein and its guanosine triphosphate exchange factor AEX‐3 confer resistance to the acute locomotor eff...

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Bibliographic Details
Published in:Genes, brain and behavior brain and behavior, 2008-08, Vol.7 (6), p.669-676
Main Authors: Kapfhamer, D., Bettinger, J. C., Davies, A. G., Eastman, C. L., Smail, E. A., Heberlein, U., McIntire, S. L.
Format: Article
Language:English
Subjects:
AEX‐3
Alcohol Drinking - genetics
Alcohol Drinking - metabolism
Alcohol Drinking - physiopathology
Alcohol-Induced Disorders, Nervous System - genetics
Alcohol-Induced Disorders, Nervous System - metabolism
Alcohol-Induced Disorders, Nervous System - physiopathology
Animals
Ataxia - chemically induced
Ataxia - genetics
Ataxia - metabolism
Behavior, Animal - drug effects
Behavior, Animal - physiology
Brain - metabolism
Brain - physiopathology
Brain Chemistry - genetics
Caenorhabditis elegans
Caenorhabditis elegans Proteins - genetics
Caenorhabditis elegans Proteins - metabolism
Central Nervous System Depressants - pharmacology
Consciousness Disorders - chemically induced
Consciousness Disorders - genetics
Consciousness Disorders - metabolism
Drug Resistance - genetics
Ethanol - pharmacology
ethanol consumption
ethanol resistance
Haplotypes - genetics
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
neurotransmitter release
presynaptic
rab3 GTP-Binding Proteins - genetics
rab3 GTP-Binding Proteins - metabolism
rab3A GTP-Binding Protein - genetics
rab3A GTP-Binding Protein - metabolism
RAB‐3/RAB3A
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Summary:The mechanisms by which ethanol induces changes in behavior are not well understood. Here, we show that Caenorhabditis elegans loss‐of‐function mutations in the synaptic vesicle‐associated RAB‐3 protein and its guanosine triphosphate exchange factor AEX‐3 confer resistance to the acute locomotor effects of ethanol. Similarly, mice lacking one or both copies of Rab3A are resistant to the ataxic and sedative effects of ethanol, and Rab3A haploinsufficiency increases voluntary ethanol consumption. These data suggest a conserved role of RAB‐3‐/RAB3A‐regulated neurotransmitter release in ethanol‐related behaviors.
ISSN:1601-1848
1601-183X
DOI:10.1111/j.1601-183X.2008.00404.x