Cited by 103Schizophrenia research and treatmentNeuroscience and Neuropharmacology ResearchNeurotransmitter Receptor Influence on Behavior

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Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia

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Carlson, Gregory C., Talbot, Konrad, Halene, Tobias B., Gandal, Michael J., Kazi, Hala A., Schlosser, Laura, Phung, Quan H., Gur, Raquel E., Arnold, Steven E., Siegel, Steven J.·2011·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.1109625108PMC PMC3203764

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Abstract

DTNBP1 (dystrobrevin binding protein 1) is a leading candidate susceptibility gene in schizophrenia and is associated with working memory capacity in normal subjects. In schizophrenia, the encoded protein dystrobrevin-binding protein 1 (dysbindin-1) is often reduced in excitatory cortical limbic synapses. We found that reduced dysbindin-1 in mice yielded deficits in auditory-evoked response adaptation, prepulse inhibition of startle, and evoked γ-activity, similar to patterns in schizophrenia. In contrast to the role of dysbindin-1 in glutamatergic transmission, γ-band abnormalities in schizophrenia are most often attributed to disrupted inhibition and reductions in parvalbumin-positive interneuron (PV cell) activity. To determine the mechanism underlying electrophysiological deficits related to reduced dysbindin-1 and the potential role of PV cells, we examined PV cell immunoreactivity and measured changes in net circuit activity using voltage-sensitive dye imaging. The dominant circuit impact of reduced dysbindin-1 was impaired inhibition, and PV cell immunoreactivity was reduced. Thus, this model provides a link between a validated candidate gene and an auditory endophenotypes. Furthermore, these data implicate reduced fast-phasic inhibition as a common underlying mechanism of schizophrenia-associated intermediate phenotypes.

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Authors: Carlson, G. C., Talbot, K., Halene, T. B., Gandal, M. J., Kazi, H. A., Schlosser, L., Phung, Q. H., Gur, R. E., Arnold, S. E., & Siegel, S. J.
Affiliations: University of Pennsylvania (US)
ORCID: Talbot, Konrad
Halene, Tobias B.
Gandal, Michael J.
Phung, Quan H.
Gur, Raquel E.
Arnold, Steven E.
Siegel, Steven J.
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2011-10-03
Volume: 108
Issue: 43
Pages: E962-70
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.1109625108
PMC: PMC3203764
OpenAlex: W2117959142
Cited by: 103
References: 86
Citations by year: 2025: 2 · 2024: 3 · 2023: 4 · 2022: 5 · 2021: 2 · 2020: 6 · 2019: 4 · 2018: 5 · 2017: 5 · 2016: 13 · 2015: 13 · 2014: 14 · 2013: 12 · 2012: 15
FWCI: 8.97
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Deutsche Forschungsgemeinschaft (IRTG1328)
National Institutes of Health (5r01da023210-05, 5p50mh064045-10, MH64045)
National Institute of Mental Health (P50 MH-064045, MH072880, R01MH072880, P50 MH 64045)
National Institute on Drug Abuse (R01-DA023210, 5R01-DA02321002)
National Cancer Institute (P50CA084718)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords: dysbindin-1, DTNBP1, schizophrenia, parvalbumin interneurons, prepulse inhibition, gamma oscillations, glutamatergic neurotransmission, candidate susceptibility genes, endophenotypes, voltage-sensitive dye imaging
MeSH terms: Dysbindin, Animals, Carrier Proteins, Electrophysiology, Evoked Potentials, Auditory, Female, Genotype, Immunohistochemistry, Limbic System, Male, Mice, Mutant Strains, Parvalbumins, Schizophrenia, Synapses, Dystrophin-Associated Proteins, Mice

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Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia

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