Prenatal stress delays inhibitory neuron progenitor migration in the developing neocortex

Hanna E Stevens; Tina Su; Yuchio Yanagawa; Flora M Vaccarino

doi:10.1016/j.psyneuen.2012.07.011

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Prenatal stress delays inhibitory neuron progenitor migration in the developing neocortex

Journal article

Peer reviewed

Prenatal stress delays inhibitory neuron progenitor migration in the developing neocortex

Hanna E Stevens, Tina Su, Yuchio Yanagawa and Flora M Vaccarino

Psychoneuroendocrinology, Vol.38(4), pp.509-521

04/2013

DOI: 10.1016/j.psyneuen.2012.07.011

PMCID: PMC3532962

PMID: 22910687

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https://www.ncbi.nlm.nih.gov/pmc/articles/3532962View

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Abstract

Prenatal stress has been widely demonstrated to have links with behavioral problems in clinical populations and animal models, however, few investigations have examined the immediate developmental events that are affected by prenatal stress. Here, we utilize GAD67GFP transgenic mice in which GABAergic progenitors express green fluorescent protein (GFP) to examine the impact of prenatal stress on the development of these precursors to inhibitory neurons. Pregnant female mice were exposed to restraint stress three times daily from embryonic day 12 (E12) onwards. Their offspring demonstrated changes in the distribution of GFP-positive (GFP+) GABAergic progenitors in the telencephalon as early as E13 and persisting until postnatal day 0. Changes in distribution reflected alterations in tangential migration and radial integration of GFP+ cells into the developing cortical plate. Fate mapping of GAD67GFP+progenitors with bromodeoxyuridine injected at E13 demonstrated a significant increase of these cells at P0 in anterior white matter. An overall decrease in GAD67GFP+ progenitors at P0 in medial frontal cortex could not be attributed to a reduction in cell proliferation. Significant changes in dlx2, nkx2.1 and their downstream target erbb4 , transcription factors which regulate interneuron migration, were found within the prenatally-stressed developing forebrain, while no differences were seen in mash1 , a determinant of interneuron fate, bdnf , a maturation factor for GABAergic cells or fgf2 , an early growth/differentiation factor. These results demonstrate that early disruption in GABAergic progenitor migration caused by prenatal stress may be responsible for neuronal defects in disorders with GABAergic abnormalities like schizophrenia.

migration

erbb4

GAD67

transcription factors

Prenatal stress

inhibitory neurons

Details

Title: Subtitle: Prenatal stress delays inhibitory neuron progenitor migration in the developing neocortex
Creators: Hanna E Stevens - Child Study Center, Yale University, 230 South Frontage Rd, New Haven, CT O6520
Tina Su - Child Study Center, Yale University, 230 South Frontage Rd, New Haven, CT O6520
Yuchio Yanagawa - Department of Genetic and Behavioural Neuroscience, Gunma University Graduate School of Medicine, Maebashi 371-8511, Japan
Flora M Vaccarino - Child Study Center, Yale University, 230 South Frontage Rd, New Haven, CT O6520
Resource Type: Journal article
Publication Details: Psychoneuroendocrinology, Vol.38(4), pp.509-521
DOI: 10.1016/j.psyneuen.2012.07.011
PMID: 22910687
PMCID: PMC3532962
NLM abbreviation: Psychoneuroendocrinology
ISSN: 0306-4530
eISSN: 1873-3360
Grant note: R01 MH067715 || MH / National Institute of Mental Health : NIMH R25 MH077823 || MH / National Institute of Mental Health : NIMH R25 MH071584 || MH / National Institute of Mental Health : NIMH T32 MH018268 || MH / National Institute of Mental Health : NIMH
Language: English
Date published: 04/2013
Academic Unit: Psychiatry; Stead Family Department of Pediatrics; Iowa Neuroscience Institute
Record Identifier: 9984070445302771

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