Journal article
Prenatal stress alters mouse offspring dorsal striatal development and placental function in sex-specific ways
Journal of psychiatric research, Vol.182, pp.149-160
02/2025
DOI: 10.1016/j.jpsychires.2024.12.048
PMCID: PMC11959308
PMID: 39809011
Abstract
Prenatal stress is a risk factor for neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD). However, how early stress modification of brain development contributes to this pathophysiology is poorly understood. Ventral forebrain regions such as dorsal striatum are of particular interest: dorsal striatum modulates movement and cognition, is altered in NDDs, and has a primarily GABAergic population. Here, we examine effects of prenatal stress on adult movement, cognition, and dorsal striatum neurobiology in mice using striatal-dependent behavioral assays, immunohistochemistry, embryonic ventral forebrain transcriptomics, and placental transcriptomics. We found prenatal stress affected adult procedural, habit, and reversal learning in sex-specific ways. Stress also increased adult dorsal striatal GABAergic neurons – an effect largely driven by males. We sought to examine the developmental origins of these adult brain changes. We found similar sex-specific dorsal striatal cellular changes in earlier points of development. The dorsal striatum primordium--embryonic ventral forebrain—showed that prenatal stress increased DNA replication and cell cycle pathways in male but not female transcriptomics and cellular biology. Unique signatures may have arisen from male-female placental differences. Stress-induced placental transcriptomics showed upregulated morphogenesis pathways in males while females downregulated morphogenic, hormonal, and cellular response pathways. Our findings suggest that prenatal stress could affect placenta function and also alter the GABAergic population of dorsal striatum differentially between the sexes.
Details
- Title: Subtitle
- Prenatal stress alters mouse offspring dorsal striatal development and placental function in sex-specific ways
- Creators
- Sara V. Maurer - Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA 52246Benjamin W.Q. Hing - Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA 52246Stephanie Lussier - University of IowaSreya Radhakrishna - Yale School of MedicineJada L.B. Davis - Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA 52246Parker W. Abbott - University of IowaJacob J. Michaelson - University of IowaHanna E. Stevens - Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA 52246
- Resource Type
- Journal article
- Publication Details
- Journal of psychiatric research, Vol.182, pp.149-160
- DOI
- 10.1016/j.jpsychires.2024.12.048
- PMID
- 39809011
- PMCID
- PMC11959308
- NLM abbreviation
- J Psychiatr Res
- ISSN
- 0022-3956
- eISSN
- 1879-1379
- Publisher
- Elsevier Ltd
- Grant note
- NIH: R01 MH122485, K08 MH086812 Patterson TrustINSPIRE Postdoctoral Program: T32MH019113 Iowa Neuroscience Graduate Program: T32NS007421 Ida P. Haller Chair in Child PsychiatryRoy J. Carver Charitable Trust
This work was supported by NIH R01 MH122485, NIH K08 MH086812, the Patterson Trust, INSPIRE Postdoctoral Program T32MH019113, Iowa Neuroscience Graduate Program T32NS007421, Ida P. Haller Chair in Child Psychiatry, and the Roy J. Carver Charitable Trust.
- Language
- English
- Electronic publication date
- 01/01/2025
- Date published
- 02/2025
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Communication Sciences and Disorders; Molecular Physiology and Biophysics; Psychiatry; Iowa Neuroscience Institute; UI Research Foundation
- Record Identifier
- 9984772277802771
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