ArticleExperimental neurology2021
The glucocorticoid receptor specific modulator CORT108297 reduces brain pathology following status epilepticus.
Article in Experimental neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Stress and HPA axis dysfunction impact diverse epilepsy outcomes including psychiatric comorbidities and SUDEP.Epilepsy research · 2026Review
- TRIM8 Promotes Epileptiform Activity by Destabilizing the Glucocorticoid Receptor NR3C1 and Enhancing AMPA Receptor Phosphorylation.Biomedicines · 2026Article
- Early life stress influences epilepsy outcomes in mice.Epilepsy & behavior : E&B · 2025Article
- Hypothalamic-Pituitary-Adrenal Axis Dysfunction Elevates SUDEP Risk in a Sex-Specific Manner.eNeuro · 2024Article
- Hypothalamic-Pituitary-Adrenal Axis and Epilepsy.Journal of clinical neurology (Seoul, Korea) · 2024Review
- Stress-induced Neuroinflammation of the Spinal Cord is Restrained by Cort113176 (Dazucorilant), A Specific Glucocorticoid Receptor Modulator.Molecular neurobiology · 2024Article
- Molecular neurobiology of loss: a role for basolateral amygdala extracellular matrix.Molecular psychiatry · 2023Article
- Glucocorticoid Receptor and β-Catenin Interact in Prostate Cancer Cells and Their Co-Inhibition Attenuates Tumorsphere Formation, Stemness, and Docetaxel Resistance.International journal of molecular sciences · 2023Article
- Hippocampal glucocorticoid receptors modulate status epilepticus severity.Neurobiology of disease · 2023Article
- Neurovascular Development ineNeuro · 2023Article
- Impact of Raptor and Rictor Deletion on Hippocampal Pathology Following Status Epilepticus.Journal of molecular neuroscience : MN · 2022Article
- Cell type specificity of glucocorticoid signaling in the adult mouse hippocampus.Journal of neuroendocrinology · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
objectiveGlucocorticoid levels rise rapidly following status epilepticus and remain elevated for weeks after the injury. To determine whether glucocorticoid receptor activation contributes to the pathological sequelae of status epilepticus, mice were treated with a novel glucocorticoid receptor modulator, C108297.
methodsMice were treated with either C108297 or vehicle for 10 days beginning one day after pilocarpine-induced status epilepticus. Baseline and stress-induced glucocorticoid secretion were assessed to determine whether hypothalamic-pituitary-adrenal axis hyperreactivity could be controlled. Status epilepticus-induced pathology was assessed by quantifying ectopic hippocampal granule cell density, microglial density, astrocyte density and mossy cell loss. Neuronal network function was examined indirectly by determining the density of Fos immunoreactive neurons following restraint stress.
resultsTreatment with C108297 attenuated corticosterone hypersecretion after status epilepticus. Treatment also decreased the density of hilar ectopic granule cells and reduced microglial proliferation. Mossy cell loss, on the other hand, was not prevented in treated mice. C108297 altered the cellular distribution of Fos protein but did not restore the normal pattern of expression.
interpretationResults demonstrate that baseline corticosterone levels can be normalized with C108297, and implicate glucocorticoid signaling in the development of structural changes following status epilepticus. These findings support the further development of glucocorticoid receptor modulators as novel therapeutics for the prevention of brain pathology following status epilepticus.
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