Prolonged Period of Cortical Plasticity upon Redox Dysregulation in Fast-Spiking Interneurons.
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State: Public
Version: author
Serval ID
serval:BIB_CAD2CAEDEA9E
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Prolonged Period of Cortical Plasticity upon Redox Dysregulation in Fast-Spiking Interneurons.
Journal
Biological Psychiatry
ISSN
1873-2402 (Electronic)
ISSN-L
0006-3223
Publication state
Published
Issued date
2015
Peer-reviewed
Oui
Volume
78
Number
6
Pages
396-402
Language
english
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Abstract
BACKGROUND: Oxidative stress and the specific impairment of perisomatic gamma-aminobutyric acid circuits are hallmarks of the schizophrenic brain and its animal models. Proper maturation of these fast-spiking inhibitory interneurons normally defines critical periods of experience-dependent cortical plasticity.
METHODS: Here, we linked these processes by genetically inducing a redox dysregulation restricted to such parvalbumin-positive cells and examined the impact on critical period plasticity using the visual system as a model (3-6 mice/group).
RESULTS: Oxidative stress was accompanied by a significant loss of perineuronal nets, which normally enwrap mature fast-spiking cells to limit adult plasticity. Accordingly, the neocortex remained plastic even beyond the peak of its natural critical period. These effects were not seen when redox dysregulation was targeted in excitatory principal cells.
CONCLUSIONS: A cell-specific regulation of redox state thus balances plasticity and stability of cortical networks. Mistimed developmental trajectories of brain plasticity may underlie, in part, the pathophysiology of mental illness. Such prolonged developmental plasticity may, in turn, offer a therapeutic opportunity for cognitive interventions targeting brain plasticity in schizophrenia.
METHODS: Here, we linked these processes by genetically inducing a redox dysregulation restricted to such parvalbumin-positive cells and examined the impact on critical period plasticity using the visual system as a model (3-6 mice/group).
RESULTS: Oxidative stress was accompanied by a significant loss of perineuronal nets, which normally enwrap mature fast-spiking cells to limit adult plasticity. Accordingly, the neocortex remained plastic even beyond the peak of its natural critical period. These effects were not seen when redox dysregulation was targeted in excitatory principal cells.
CONCLUSIONS: A cell-specific regulation of redox state thus balances plasticity and stability of cortical networks. Mistimed developmental trajectories of brain plasticity may underlie, in part, the pathophysiology of mental illness. Such prolonged developmental plasticity may, in turn, offer a therapeutic opportunity for cognitive interventions targeting brain plasticity in schizophrenia.
Keywords
Adaptation, Physiological, Animals, Extracellular Matrix/metabolism, GABAergic Neurons/metabolism, GABAergic Neurons/physiology, Glutamate-Cysteine Ligase/genetics, Interneurons/metabolism, Mice, Inbred C57BL, Microglia/metabolism, Neuronal Plasticity, Oxidation-Reduction, Oxidative Stress, Parvalbumins, Sensory Deprivation/physiology, Visual Cortex/metabolism, Visual Cortex/physiology
Pubmed
Web of science
Create date
17/03/2015 15:53
Last modification date
20/08/2019 16:45