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Published on: February 6, 2015
Behavioral Characterization of β-Arrestin 1 Knockout Mice in Anxiety-Like and Alcohol Behaviors
Meridith T Robins1, Terrance Chiang1, Jennifer N Berry1
1Department of Medicinal Chemistry and Molecular Pharmacology, Purdue Institute for Integrative Neuroscience, Purdue University, West Lafayette, IN, United States.
Abstract:
β-Arrestin 1 and 2 are highly expressed proteins involved in the desensitization of G protein-coupled receptor signaling which also regulate a variety of intracellular signaling pathways. Gene knockout (KO) studies suggest that the two isoforms are not homologous in their effects on baseline and drug-induced behavior; yet, the role of β-arrestin 1 in the central nervous system has been less investigated compared to β-arrestin 2. Here, we investigate how global β-arrestin 1 KO affects anxiety-like and alcohol-related behaviors in male and female C57BL/6 mice. We observed increased baseline locomotor activity in β-arrestin 1 KO animals compared with wild-type (WT) or heterozygous (HET) mice with a sex effect. KO male mice were less anxious in a light/dark transition test, although this effect may have been confounded by increased locomotor activity. No differences in sucrose intake were observed between genotypes or sexes. Female β-arrestin 1 KO mice consumed more 10% alcohol than HET females in a limited 4-h access, two-bottle choice, drinking-in-the-dark model. In a 20% alcohol binge-like access model, female KO animals consumed significantly more alcohol than HET and WT females. A significant sex effect was observed in both alcohol consumption models, with female mice consuming greater amounts of alcohol than males relative to body weight. Increased sensitivity to latency to loss of righting reflex (LORR) was observed in β-arrestin 1 KO mice although no differences were observed in duration of LORR. Overall, our efforts suggest that β-arrestin 1 may be protective against increased alcohol consumption in females and hyperactivity in both sexes.
Insights
Beta-arrestin 1 knockout mice exhibit hyperactivity and altered anxiety-like behaviors. Female knockout mice show increased alcohol consumption, suggesting beta-arrestin 1 may protect against excessive drinking and hyperactivity.
Area of Science:
- Neuroscience
- Pharmacology
- Genetics
Background:
- Beta-arrestin 1 and 2 are key regulators of G protein-coupled receptor signaling.
- While beta-arrestin 2's CNS role is studied, beta-arrestin 1's function remains less understood.
- Gene knockout studies indicate distinct roles for beta-arrestin 1 and 2 in behavior.
Purpose of the Study:
- To investigate the impact of global beta-arrestin 1 knockout on anxiety-like and alcohol-related behaviors in male and female mice.
- To compare the behavioral phenotypes of beta-arrestin 1 knockout mice with wild-type and heterozygous controls.
- To explore potential sex-specific effects of beta-arrestin 1 deficiency on behavior.
Main Methods:
- Global beta-arrestin 1 knockout (KO), heterozygous (HET), and wild-type (WT) C57BL/6 mice were used.
- Behavioral tests included locomotor activity, light/dark transition test, sucrose intake, and alcohol consumption (two-bottle choice, drinking-in-the-dark).
- Sensitivity to alcohol was assessed by latency to loss of righting reflex (LORR).
Main Results:
- Beta-arrestin 1 KO mice displayed increased baseline locomotor activity, with a significant sex effect.
- Male KO mice showed reduced anxiety in the light/dark test, potentially confounded by hyperactivity.
- Female KO mice consumed significantly more alcohol than controls in both limited and binge-access models, with females showing higher relative consumption than males.
- KO mice exhibited increased sensitivity to alcohol's intoxicating effects (decreased LORR latency).
Conclusions:
- Beta-arrestin 1 deficiency leads to hyperactivity in both sexes and increased alcohol consumption specifically in females.
- These findings suggest beta-arrestin 1 may play a protective role against excessive alcohol intake in females and hyperactivity.
- Further research into beta-arrestin 1's central nervous system functions is warranted.
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