ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Glucocorticoid suppresses dendritic spine development mediated by down-regulation of caldesmon expression.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Defining functional states and roles of microglia in neuropsychiatric disorders.Frontiers in cellular neuroscience · 2026Review
- Stress in utero: prenatal dexamethasone exposure causes greater structural gliovascular alterations in female offspring than in males.Frontiers in neuroscience · 2025Article
- Gene expression in the primate orbitofrontal cortex related to anxious temperament.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Contribution of AMPA Receptor-Mediated LTD in LA/BLA-CeA Pathway to Comorbid Aversive and Depressive Symptoms in Neuropathic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Resilience to stress and sex-specific remodeling of microglia and neuronal morphology in a rat model of anxiety and anhedonia.Neurobiology of stress · 2021Article
- Hemmule: A Novel Structure with the Properties of the Stem Cell Niche.International journal of molecular sciences · 2020Article
- Selective activation of parvalbumin interneurons prevents stress-induced synapse loss and perceptual defects.Molecular psychiatry · 2018Article
- IL-1β suppresses cLTP-induced surface expression of GluA1 and actin polymerization via ceramide-mediated Src activation.Journal of neuroinflammation · 2018Article
- Genome-wide Methyl-Seq analysis of blood-brain targets of glucocorticoid exposure.Epigenetics · 2017Article
- Adenosine AMolecular psychiatry · 2017Article
- Article
- Prolonged corticosterone exposure induces dendritic spine remodeling and attrition in the rat medial prefrontal cortex.The Journal of comparative neurology · 2016Article
- Tumor Necrosis Factor-α Underlies Loss of Cortical Dendritic Spine Density in a Mouse Model of Congestive Heart Failure.Journal of the American Heart Association · 2015Article
- Adrenocortical status predicts the degree of age-related deficits in prefrontal structural plasticity and working memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- New insight on the molecular aspects of glucocorticoid effects in nervous system development.Journal of endocrinological investigation · 2013Review
- Chronic stress-induced alterations of dendritic spine subtypes predict functional decrements in an hypothalamo-pituitary-adrenal-inhibitory prefrontal circuit.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Molecular mechanisms of dendrite stability.Nature reviews. Neuroscience · 2013Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids (GCs) mediate the effects of stress to cause structural plasticity in brain regions such as the hippocampus, including simplification of dendrites and shrinkage of dendritic spines. However, the molecular mechanics linking stress and GCs to these effects remain largely unclear. Here, we demonstrated that corticosterone (CORT) reduces the expression levels of caldesmon (CaD), causing dendritic spines to become vulnerable. CaD regulates cell motility by modulating the actin-myosin system and actin filament stability. In cultured rat hippocampal neurons, CaD localized to dendritic spines by binding to filamentous actin (F-actin), and CaD expression levels increased during spine development. CaD stabilized the F-actin dynamics in spines, thereby enlarging the spine heads, whereas CaD knockdown decreased the spine-head size via destabilization of the F-actin dynamics. CaD was also required for chemical LTP-induced actin stabilization. The CaD expression levels were markedly decreased by exposure to CORT mediated by suppression of serum response factor-dependent transcription. High CORT levels reduced both the spine-head size and F-actin stability similarly to CaD knockdown, and overexpressing CaD abolished the detrimental effect of CORT on dendritic spine development. These results indicate that CaD enlarges the spine-head size by stabilizing F-actin dynamics, and that CaD is a critical target in the GC-induced detrimental effects on dendritic spine development.
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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.