ArticleBehavioural brain research2013
Loss of dysbindin-1 in mice impairs reward-based operant learning by increasing impulsive and compulsive behavior.
Article in Behavioural brain research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Dysbindin-1, BDNF, and GABAergic Transmission in Schizophrenia.Frontiers in psychiatry · 2022Review
- Histone deacetylase-3: Friend and foe of the brain.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- Retinal biomarkers and pharmacological targets for Hermansky-Pudlak syndrome 7.Scientific reports · 2020Article
- Impaired copper transport in schizophrenia results in a copper-deficient brain state: A new side to the dysbindin story.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2020Article
- Loss of dysbindin-1 affects GABAergic transmission in the PFC.Psychopharmacology · 2019Article
- Deletion of Dtnbp1 in mice impairs threat memory consolidation and is associated with enhanced inhibitory drive in the amygdala.Translational psychiatry · 2019Article
- Developmental Genes and Regulatory Proteins, Domains of Cognitive Impairment in Schizophrenia Spectrum Psychosis and Implications for Antipsychotic Drug Discovery: The Example of Dysbindin-1 Isoforms and Beyond.Frontiers in pharmacology · 2019Review
- An Overview of Animal Models Related to Schizophrenia.Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2019Review
- Sleep/Wake Disruption in a Mouse Model of BLOC-1 Deficiency.Frontiers in neuroscience · 2018Article
- Translating advances in the molecular basis of schizophrenia into novel cognitive treatment strategies.British journal of pharmacology · 2017Review
- Dysbindin-1 Involvement in the Etiology of Schizophrenia.International journal of molecular sciences · 2017Review
- Disrupted-in-schizophrenia 1 (DISC1) regulates dysbindin function by enhancing its stability.The Journal of biological chemistry · 2015Article
- Behavioral characterization of mice overexpressing human dysbindin-1.Molecular brain · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The dystrobrevin-binding protein 1 (DTNBP1) gene, which encodes the dysbindin-1 protein, is a potential schizophrenia susceptibility gene. Polymorphisms in the DTNBP1 gene have been associated with altered cognitive abilities. In the present study, dysbindin-1 null mutant (dys-/-), heterozygous (dys+/-), and wild-type (dys+/+) mice, on a C57BL/6J genetic background, were tested in either a match to sample or nonmatch to sample visual discrimination task. This visual discrimination task was designed to measure rule learning and detect any changes in response timing over the course of testing. Dys-/- mice displayed significant learning deficits and required more trials to acquire this task. However, once criterion was reached, there were no differences between the genotypes on any behavioral measures. Dys-/- mice exhibited increased compulsive and impulsive behaviors compared to control littermates suggesting the inability to suppress incorrectly-timed responses underlies their increased time to acquisition. Indeed, group comparisons of behavior differences between the first and last day of testing showed that only dys-/- mice consistently decreased measures of perseverative, premature, timeout, and total responses. These findings illustrate how some aspects of altered cognitive performance in dys-/- mice might be related to increased impulsive and compulsive behaviors, analogous to cognitive deficits in some individuals with psychiatric disorders.
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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.