ArticleNeuroscience bulletin2013
β-Arrestin-2 inhibits preference for alcohol in mice and suppresses Akt signaling in the dorsal striatum.
Article in Neuroscience bulletin, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Deletion of arrestin-3 does not reduce drug-seeking behavior in a longitudinal paradigm of oral morphine self-administration.Frontiers in pharmacology · 2024Article
- A systems omics-based approach to decode substance use disorders and neuroadaptations.Neuroscience and biobehavioral reviews · 2021Review
- Normal Ethanol Sensitivity and Rapid Tolerance Require the G Protein Receptor Kinase 2 in Ellipsoid Body Neurons in Drosophila.Alcoholism, clinical and experimental research · 2020Article
- Critical Role for GFrontiers in psychiatry · 2018Article
- Arresting the Development of Addiction: The Role ofThe Journal of pharmacology and experimental therapeutics · 2017Review
- Down-regulation of β-arrestin2 promotes tumour invasion and indicates poor prognosis of hepatocellular carcinoma.Scientific reports · 2016Article
- Genes and Alcohol Consumption: Studies with Mutant Mice.International review of neurobiology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we investigated the role of β-arrestin-2 in alcohol preference using the two-bottle choice and conditioned place preference procedures in wild-type (WT) and β-arrestin-2 knockout (KO) mice. Locomotion and righting reflex tests were performed to test alcohol sensitivity. The possible molecular signals regulated by β-arrestin-2 were analyzed by Western blot. We found that β-arrestin-2 KO mice showed a marked increase in voluntary alcohol consumption without significant differences in preference for saccharin or aversion to quinine. These animals also exhibited higher conditioned place preference scores for alcohol than WT mice. Meanwhile, KO mice showed reduced sensitivity to alcohol and increased blood alcohol clearance. Furthermore, after the free consumption of alcohol, the activities of protein kinase B and glycogen synthase kinase 3β (GSK3β) increased in the dorsal striatum of WT mice, but not in KO mice, which showed high basal activity of Akt in the dorsal striatum. These results suggest that β-arrestin-2 negatively regulates alcohol preference and reward, likely through regulating the activation of signaling pathways including Akt/GSK3β in the dorsal striatum.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.