ArticleMolecular psychiatry2009
Detrimental effects of glucocorticoids on neuronal migration during brain development.
Article in Molecular psychiatry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 96 citations in OpenAlex.
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- Defining functional states and roles of microglia in neuropsychiatric disorders.Frontiers in cellular neuroscience · 2026Review
- Effect of Corticosterone on Gene Expression in the Context of Global Hippocampal Transcription.International journal of molecular sciences · 2025Article
- Stress in utero: prenatal dexamethasone exposure causes greater structural gliovascular alterations in female offspring than in males.Frontiers in neuroscience · 2025Article
- The role of zinc in the premature brain: functions, outcomes and future research perspectives.Frontiers in pediatrics · 2024Review
- Glucocorticoid receptor-induced non-muscle caldesmon regulates metastasis in castration-resistant prostate cancer.Oncogenesis · 2023Article
- Overnight Corticosterone and Gene Expression in Mouse Hippocampus: Time Course during Resting Period.International journal of molecular sciences · 2023Article
- Caldesmon controls stress fiber force-balance through dynamic cross-linking of myosin II and actin-tropomyosin filaments.Nature communications · 2022Article
- Antenatal Dexamethasone Treatment Induces Sex-dependent Upregulation of NTPDase1/CD39 and Ecto-5'-nucleotidase/CD73 in the Rat Fetal Brain.Cellular and molecular neurobiology · 2022Article
- Neurodevelopmental signatures of narcotic and neuropsychiatric risk factors in 3D human-derived forebrain organoids.Molecular psychiatry · 2021Article
- Experience and activity-dependent control of glucocorticoid receptors during the stress response in large-scale brain networks.Stress (Amsterdam, Netherlands) · 2021Article
- Neurobiology of zinc and its role in neurogenesis.European journal of nutrition · 2021Review
- Cellular stress mechanisms of prenatal maternal stress: Heat shock factors and oxidative stress.Neuroscience letters · 2019Review
- Social Stress-Induced Postsynaptic Hyporesponsiveness in Glutamatergic Synapses Is Mediated by PSD-Zip70-Rap2 Pathway and Relates to Anxiety-Like Behaviors.Frontiers in cellular neuroscience · 2019Article
- Adverse neuropsychiatric development following perinatal brain injury: from a preclinical perspective.Pediatric research · 2019Review
- Prenatal Environment That Affects Neuronal Migration.Frontiers in cell and developmental biology · 2019Review
- Maternal hormonal milieu influence on fetal brain development.Brain and behavior · 2018Review
- The contribution of 7q33 copy number variations for intellectual disability.Neurogenetics · 2018Article
- Nuclear receptors in neural stem/progenitor cell homeostasis.Cellular and molecular life sciences : CMLS · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids, the most downstream effectors of the hypothalamus-pituitary-adrenal axis, are one of main mediators of the stress reaction. Indeed, exposure to high levels of stress-triggered glucocorticoids is detrimental to brain development associated with abnormal behaviors in experimental animals and the risk of psychiatric disorders in humans. Despite the wealth of this knowledge, the cellular and molecular mechanisms underlying the detrimental effects of glucocorticoids on brain development remain unclear. Here, we show that excess glucocorticoids retard the radial migration of post-mitotic neurons during the development of the cerebral cortex, and identify an actin regulatory protein, caldesmon, as the glucocorticoids' main target. The upregulation of caldesmon expression is mediated by glucocorticoid receptor-dependent transcription of the CALD1 gene encoding caldesmon. This upregulated caldesmon negatively controls the function of myosin II, leading to changes in cell shape and migration. The depletion of caldesmon in vivo impairs radial migration. The overexpression of caldesmon also causes delayed radial migration during cortical development, mimicking the excessive glucocorticoid-induced retardation of radial migration. We conclude that an appropriate range of caldesmon expression is critical for radial migration, and that its overexpression induced by excess glucocorticoid retards radial migration during cortical development. Thus, this study provides a novel insight into the underlying mechanism of glucocorticoid-related neurodevelopmental disorders.
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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.