The DOI matches its Crossref record; 85 of the 86 references it cites were found in a registry or an index.
Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia
Open accessAbstract
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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“Recent studies have revealed anomalies in hippocampal and/or prefrontal PVI in many preclinical animal models aiming to reproduce genetic vulnerabilities (Carlson et al., 2011; Fazzari et al., 2010; Hikida et al., 2007; Wen et al., 2010) or environmental risk factors (Brown, 2011) such as prenatal maternal stress (Stevens et al., 2013), maternal and perinatal immune challenge (Jenkins et al., 2009”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Carlson et al., 2011
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- 10.1038/sj.mp.4001558 · DOI · Paper page
- 10.1172/JCI200420425 · DOI
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Crown, L. M., Featherstone, R. E., Sobell, J. L., Parekh, K., & Siegel, S. J. (2024) · Advances in neurobiology · doi:10.1007/978-3-031-69491-2_11
Self-citationSleep-wake regulation by Palladin via the blood-brain-barrier
Li, H. (2022) · theses.fr (ABES) · doi:10.70675/6142554dzdf7dz4640z8c76ze90c5609291d
Metadata
- 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
- 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
- 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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