Multiple origins of the cortical gamma rhythm
Open accessAbstract
Gamma rhythms (30–80 Hz) are a near‐ubiquitous feature of neuronal population activity in mammalian cortices. Their dynamic properties permit the synchronization of neuronal responses to sensory input within spatially distributed networks, transient formation of local neuronal “cell assemblies,” and coherent response patterns essential for intercortical regional communication. Each of these phenomena form part of a working hypothesis for cognitive function in cortex. All forms of physiological gamma rhythm are inhibition based, being characterized by rhythmic trains of inhibitory postsynaptic potentials in populations of principal neurons. It is these repeating periods of relative enhancement and attenuation of the responsivity of major cell groups in cortex that provides a temporal structure shared across many millions of neurons. However, when considering the origins of these repeating trains of inhibitory events considerable divergence is seen depending on cortical region studied and mode of activation of gamma rhythm generating networks. Here, we review the evidence for involvement of multiple subtypes of interneuron and focus on different modes of activation of these cells. We conclude that most massively parallel brain regions have different mechanisms of gamma rhythm generation, that different mechanisms have distinct functional correlates, and that switching between different local modes of gamma generation may be an effective way to direct cortical communication streams. Finally, we suggest that developmental disruption of the endophenotype for certain subsets of gamma‐generating interneuron may underlie cognitive deficit in psychiatric illness. © 2010 Wiley Periodicals, Inc. Develop Neurobiol 71: 92–106, 2011
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Ketamine induces superoxide overproduction that strongly impairs PV cells, causing loss of normal phenotype including PV immunoreactivity but without cell death.
“For instance, ketamine induces superoxide overproduction that strongly impairs PV cells (i.e., loss of normal phenotype including PV immunoreactivity but without cell death) (4,5).”
From Perineuronal nets protect fast-spiking interneurons against oxidative stress (2013) · cites this paper as [4]
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References 107 · Cited by 253
- Authors
- Whittington, M. A., Cunningham, M. O., LeBeau, F. E. N., Racca, C., & Traub, R. D.
- Affiliations
- Newcastle University (GB)
- IBM Research - Thomas J. Watson Research Center (US)
- Corresponding author
- Whittington, Miles A.
- Venue
- Developmental Neurobiology
- Publisher
- Wiley
- Published
- 2010-12-11
- Volume
- 71
- Issue
- 1
- Pages
- 92-106
- ISSN
- 1932-8451 (ISSN-L)
- 1932-846X
- OpenAlex
- W2058184445
- Cited by
- 253
- References
- 107
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 9 · 2023: 13 · 2022: 17 · 2021: 12 · 2020: 15 · 2019: 11 · 2018: 22 · 2017: 18 · 2016: 26 · 2015: 22 · 2014: 12 · 2013: 25 · 2012: 26
- FWCI
- 12.80
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- Developmental Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- Wellcome Trust
- National Institutes of Health (5r01ns044133-15)
- National Institute of Neurological Disorders and Stroke (R01-NS044133)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- interneurons, inhibitory postsynaptic potentials, neuronal synchronization, cell assemblies, interneuron subtypes, developmental disruption, mental illness, cognitive impairment, endophenotypes
- MeSH terms
- Animals, Biological Clocks, Cerebral Cortex, Cortical Synchronization, Humans, Interneurons, Nerve Net, Brain Waves
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