ArticleNeuroscience2011
Dexamethasone induces apoptosis in the developing rat amygdala in an age-, region-, and sex-specific manner.
Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 62 citations in OpenAlex.
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- Impact of Antenatal Corticosteroids on Brain Function and Underlying Mechanisms in Preclinical Studies: Protocol for a Systematic Review.JMIR research protocols · 2026Article
- From Formulation to Function: γ‑Oryzanol Solid Dispersion Development and Its Neuroprotective Effects on the Depression Model.ACS omega · 2025Article
- Maternal immune activation with toll-like receptor 7 agonist during mid-gestation alters juvenile and adult developmental milestones and behavior.Journal of neuroendocrinology · 2024Article
- Brain effects of gestating germ-free persist in mouse neonates despite acquisition of a microbiota at birth.Frontiers in neuroscience · 2023Article
- Antenatal PPAR-γ agonist pioglitazone stimulates fetal lung maturation equally in males and females.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Roles for androgens in mediating the sex differences of neuroendocrine and behavioral stress responses.Biology of sex differences · 2020Review
- Sex differences in major depression and comorbidity of cardiometabolic disorders: impact of prenatal stress and immune exposures.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Review
- Birth delivery mode alters perinatal cell death in the mouse brain.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Stress in Regulation of GABA Amygdala System and Relevance to Neuropsychiatric Diseases.Frontiers in neuroscience · 2018Review
- The microbiota influences cell death and microglial colonization in the perinatal mouse brain.Brain, behavior, and immunity · 2018Article
- The role of IL-6 in neurodevelopment after prenatal stress.Brain, behavior, and immunity · 2017Article
- Minocycline causes widespread cell death and increases microglial labeling in the neonatal mouse brain.Developmental neurobiology · 2017Article
- Patterns of cell death in the perinatal mouse forebrain.The Journal of comparative neurology · 2017Article
- Modulation of the Hypothalamic-Pituitary-Adrenal Axis by Early Life Stress Exposure.Frontiers in cellular neuroscience · 2017Review
- Counteractive effects of antenatal glucocorticoid treatment on D1 receptor modulation of spatial working memory.Psychopharmacology · 2016Article
- Sex-dependent programming effects of prenatal glucocorticoid treatment on the developing serotonin system and stress-related behaviors in adulthood.Neuroscience · 2016Article
- Sex differences, hormones, and fMRI stress response circuitry deficits in psychoses.Psychiatry research · 2015Article
- Maternal treatment with glucocorticoids modulates gap junction protein expression in the ovine fetal brain.Neuroscience · 2014Article
- Prenatal stress and inhibitory neuron systems: implications for neuropsychiatric disorders.Molecular psychiatry · 2014Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Exposure to glucocorticoids (GCs) in early development can lead to long-term changes in brain function and behavior, although little is known about the underlying neural mechanisms. Perinatal exposure to GCs alters adult anxiety and neuroendocrine responses to stress. Therefore, we investigated the effects of either late gestational or neonatal exposure to the GC receptor agonist dexamethasone (DEX), on apoptosis within the amygdala, a region critical for emotional regulation. DEX was administered to timed-pregnant rat dams from gestational day 18 until parturition, or postnatal day 4-6. Offspring were sacrificed the day following the last DEX treatment, and tissue was processed for immunohistochemical detection of cleaved caspase-3, a marker for apoptotic cells. Prenatal DEX treatment significantly increased the number of cleaved caspase-3-positive cells in the amygdala of both sexes, largely due to increases within the medial and basomedial subregions. Postnatal DEX treatment also increased cleaved caspase-3 immunoreactivity within the amygdala, although effects reached significance only in the central nucleus of females. Overall, DEX induction of cleaved caspase-3 in the amygdala was greater following prenatal compared with postnatal treatment, yet in both instances, elevations in cleaved caspase-3 correlated with an increase in pro-apoptotic Bax mRNA expression. Dual-label immunohistochemistry of cleaved caspase-3 and the neuronal marker NeuN confirmed that virtually all cleaved caspase-3-positive cells in the amygdala were neurons, and a subset of these cells (primarily following postnatal treatment) expressed a GABAergic calcium-binding protein phenotype (calbindin or calretinin). Together these results indicate that early developmental GC exposure induces neuronal apoptosis within the amygdala in an age-, sex-, and region-dependent manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.