Journal article
The Role of Redox Dysregulation in the Effects of Prenatal Stress on Embryonic Interneuron Migration
Cerebral cortex (New York, N.Y. 1991), Vol.29(12), pp.5116-5130
12/17/2019
DOI: 10.1093/cercor/bhz052
PMID: 30877797
Abstract
Abstract Maternal stress during pregnancy is associated with increased risk of psychiatric disorders in offspring, but embryonic brain mechanisms disrupted by prenatal stress are not fully understood. Our lab has shown that prenatal stress delays inhibitory neural progenitor migration. Here, we investigated redox dysregulation as a mechanism for embryonic cortical interneuron migration delay, utilizing direct manipulation of pro- and antioxidants and a mouse model of maternal repetitive restraint stress starting on embryonic day 12. Time-lapse, live-imaging of migrating GAD67GFP+ interneurons showed that normal tangential migration of inhibitory progenitor cells was disrupted by the pro-oxidant, hydrogen peroxide. Interneuron migration was also delayed by in utero intracerebroventricular rotenone. Prenatal stress altered glutathione levels and induced changes in activity of antioxidant enzymes and expression of redox-related genes in the embryonic forebrain. Assessment of dihydroethidium (DHE) fluorescence after prenatal stress in ganglionic eminence (GE), the source of migrating interneurons, showed increased levels of DHE oxidation. Maternal antioxidants (N-acetylcysteine and astaxanthin) normalized DHE oxidation levels in GE and ameliorated the migration delay caused by prenatal stress. Through convergent redox manipula-tions, delayed interneuron migration after prenatal stress was found to critically involve redox dysregulation. Redox biology during prenatal periods may be a target for protecting brain development.
Details
- Title: Subtitle
- The Role of Redox Dysregulation in the Effects of Prenatal Stress on Embryonic Interneuron Migration
- Creators
- Jada Bittle - Department of Psychiatry, University of Iowa Carver College of Medicine, 1310 PBDB, 169 Newton Rd, Iowa City, IA, USA, Interdisciplinary Graduate Program in Neuroscience, University of Iowa, 356 Medical Research Center, Iowa City, IA, USAEdenia C Menezes - Department of Psychiatry, University of Iowa Carver College of Medicine, 1310 PBDB, 169 Newton Rd, Iowa City, IA, USAMichael L McCormick - Free Radical and Radiation Biology Program, Department of Radiation Oncology, University of Iowa Carver College of Medicine, B180 Medical Laboratories, Iowa City, IA, USADouglas R Spitz - Free Radical and Radiation Biology Program, Department of Radiation Oncology, University of Iowa Carver College of Medicine, B180 Medical Laboratories, Iowa City, IA, USAMichael Dailey - Interdisciplinary Graduate Program in Neuroscience, University of Iowa, 356 Medical Research Center, Iowa City, IA, USA, Iowa Neuroscience Institute, University of Iowa, 2312 PBDB, 169 Newton Rd, Iowa City, IA, USAHanna E Stevens - Department of Psychiatry, University of Iowa Carver College of Medicine, 1310 PBDB, 169 Newton Rd, Iowa City, IA, USA, Interdisciplinary Graduate Program in Neuroscience, University of Iowa, 356 Medical Research Center, Iowa City, IA, USA, Iowa Neuroscience Institute, University of Iowa, 2312 PBDB, 169 Newton Rd, Iowa City, IA, USA
- Resource Type
- Journal article
- Publication Details
- Cerebral cortex (New York, N.Y. 1991), Vol.29(12), pp.5116-5130
- DOI
- 10.1093/cercor/bhz052
- PMID
- 30877797
- NLM abbreviation
- Cereb Cortex
- ISSN
- 1047-3211
- eISSN
- 1460-2199
- Grant note
- DOI: 10.13039/100012138, name: Nellie Ball Trust; DOI: 10.13039/100001024, name: Roy J. Carver Charitable Trust; DOI: 10.13039/100008893, name: University of Iowa; DOI: 10.13039/100000002, name: National Institutes of Health, award: T32NS007421
- Language
- English
- Date published
- 12/17/2019
- Academic Unit
- Psychiatry; Stead Family Department of Pediatrics; Pathology; Iowa Neuroscience Institute; Biology; Radiation Oncology
- Record Identifier
- 9983992061302771
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