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Alterations of Cortical GABA Neurons and Network Oscillations in Schizophrenia
Open accessAbstract
The hypothesis that alterations of cortical inhibitory gamma-aminobutyric acid (GABA) neurons are a central element in the pathology of schizophrenia has emerged from a series of postmortem studies. How such abnormalities may contribute to the clinical features of schizophrenia has been substantially informed by a convergence with basic neuroscience studies revealing complex details of GABA neuron function in the healthy brain. Importantly, activity of the parvalbumin-containing class of GABA neurons has been linked to the production of cortical network oscillations. Furthermore, growing knowledge supports the concept that gamma band oscillations (30-80 Hz) are an essential mechanism for cortical information transmission and processing. Herein we review recent studies further indicating that inhibition from parvalbumin-positive GABA neurons is necessary to produce gamma oscillations in cortical circuits; provide an update on postmortem studies documenting that deficits in the expression of glutamic acid decarboxylase67, which accounts for most GABA synthesis in the cortex, are widely observed in schizophrenia; and describe studies using novel, noninvasive approaches directly assessing potential relations between alterations in GABA, oscillations, and cognitive function in schizophrenia.
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“its onset is linked to a potential disruption of the physiological maturation of inhibitory neural networks consisting of fast-spiking parvalbumin-positive gamma-aminobutric acid (GABAergic) interneurons”
From Perineuronal nets and schizophrenia: The importance of neuronal coatings (2014) · cites this paper as Gonzalez-Burgos et al., 2010
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Metadata
- Authors
- Gonzalez-Burgos, G., Hashimoto, T., & Lewis, D. A.
- Affiliations
- Kanazawa University (JP)
- University of Pittsburgh (US)
- Venue
- Current Psychiatry Reports
- Published
- 2010-06-17
- Volume
- 12
- Issue
- 4
- Pages
- 335-344
- ISSN
- 1523-3812 (ISSN-L)
- 1535-1645
- PMC
- PMC2919752
- OpenAlex
- W2073239561
- Cited by
- 260
- References
- 97
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 10 · 2023: 11 · 2022: 9 · 2021: 10 · 2020: 12 · 2019: 8 · 2018: 9 · 2017: 15 · 2016: 14 · 2015: 21 · 2014: 21 · 2013: 30 · 2012: 29
- FWCI
- 4.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Current Psychiatry Reports (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (P50MH084053, R01MH051234)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- schizophrenia, GABAergic neurons, parvalbumin, gamma oscillations, cortical inhibition, glutamic acid decarboxylase 67, postmortem brain studies, cognitive function
- MeSH terms
- Biological Clocks, Cerebral Cortex, gamma-Aminobutyric Acid, Humans, Nerve Net, Synaptic Transmission, Neurons, Schizophrenia
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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