Interneuron epigenomes during the critical period of cortical plasticity: Implications for schizophrenia
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Schizophrenia, a major psychiatric disorder defined by delusions and hallucinations, among other symptoms, often with onset in early adulthood, is potentially associated with molecular and cellular alterations in parvalbumin-expressing fast spiking interneurons and other constituents of the cortical inhibitory GABAergic circuitry. The underlying mechanisms, including the role of disease-associated risk factors operating in adolescence such as drug abuse and social stressors, remain incompletely understood. Here, we summarize emerging findings from animal models, highlighting the ability of parvalbuminergic interneurons (PVI) to induce, during the juvenile period, long-term plastic changes in prefrontal and visual cortex, thereby altering perception, cognition and behavior in the adult. Of note, molecular alterations in PVI from subjects with schizophrenia, including downregulated expression of a subset of GABAergic genes, have also been found in juvenile stress models of the disorder. Some of the transcriptional alterations observed in schizophrenia postmortem brain could be linked to changes in the epigenetic architecture of GABAergic gene promoters, including dysregulated DNA methylation, histone modification patterns and disruption of promoter-enhancer interactions at site of chromosomal loop formations. Therefore, we predict that, in the not-to-distant future, PVI- and other cell-type specific epigenomic mappings in the animal model and human brain will provide novel insights into the pathophysiology of schizophrenia and related psychotic diseases, including the role of cortical GABAergic circuitry in shaping long-term plasticity and cognitive function of the cerebral cortex.
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Redox dysregulation/oxidative stress halts normal PVI maturation in the prefrontal cortex without causing their death, possibly via epigenetic mechanisms.
“Based on the fact that a peripubertal antioxidant treatment can abolish oxidative stress and rescue PVI/PNN deficit in the NVHL rat model,41 we propose a hypothesis in which redox dysregulation/oxidative stress halts normal PVI maturation in the prefrontal cortex without causing their death,82 possibly via epigenetic mechanisms.102, 103”
From Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia (2017) · cites this paper as [103]
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Research works printed but not linked: 2
- Aberg KA McClay JL Nerella S Clark S Kumar G Chen W Khachane AN Xie L Hudson A Gao G Harada A Hultman CM Sullivan PF Magnusson PK van den Oord EJ 2014 Methylome-Wide Association Study of Schizophrenia: Identifying Blood Biomarker Signatures of Environmental Insults JAMA Psychiatry PMC4331014 24402055
- Volk DW Matsubara T Li S Sengupta EJ Georgiev D Minabe Y Sampson A Hashimoto T Lewis DA 2012b Deficits in Transcriptional Regulators of Cortical Parvalbumin Neurons in Schizophrenia Am J Psychiatry PMC3513625 22983435
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Hanamsagar, R., Alter, M. D., Block, C. S., Sullivan, H., Bolton, J. L., & Bilbo, S. D. (2017) · Glia · doi:10.1002/glia.23176 · Cited by 384 · see citing works
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Self-citationCortical interneuron specification: the juncture of genes, time and geometry
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- Authors
- Morishita, H., Kundakovic, M., Bicks, L., Mitchell, A., & Akbarian, S.
- Affiliations
- Child Health and Development Institute (US)
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Morishita, Hirofumi
- Akbarian, Schahram
- Venue
- Neurobiology of Learning and Memory
- Publisher
- Elsevier BV
- Published
- 2015-10
- Volume
- 124
- Pages
- 104-110
- ISSN
- 1074-7427 (ISSN-L)
- PMC
- PMC4568154
- OpenAlex
- W2086743087
- Cited by
- 42
- References
- 112
- Citations by year
- 2025: 3 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 5 · 2019: 3 · 2018: 6 · 2017: 8 · 2016: 7 · 2015: 3
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Learning and Memory (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Brain and Behavior Research Foundation
- Brain Research Foundation
- National Institutes of Health
- National Institute of Mental Health (T32MH096678, R01MH093332, T32MH087004)
- 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 › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- schizophrenia, parvalbumin interneurons, cortical plasticity, critical period, epigenetics, DNA methylation, histone modifications, enhancer-promoter interactions, chromatin looping, juvenile stress, drug abuse, prefrontal cortex, visual cortex
- MeSH terms
- Animals, Cerebral Cortex, Disease Models, Animal, Glutamate Decarboxylase, Humans, Interneurons, Neuronal Plasticity, Parvalbumins, Schizophrenia, Time Factors, Visual Cortex, Prefrontal Cortex, DNA Methylation, Epigenesis, Genetic, GABAergic Neurons
About these checks
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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