ArticleInternational journal of molecular sciences2022
Effects of RU486 in Treatment of Traumatic Stress-Induced Glucocorticoid Dysregulation and Fear-Related Abnormalities: Early versus Late Intervention.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Mifepristone as a pharmacological intervention for stress-induced alcohol craving: A human laboratory study.Addiction biology · 2023Trial
- Traditional Fermented Multi-Grain Supernatant (Ogi-baba Omidun) Restores Hypothalamic-Pituitary-Testicular Axis Function in a Juvenile Double-Hit PTSD-Neuroinflammation Rat Model.Molecular neurobiology · 2026Article
- Review
- Transcriptional changes across tissue and time provide molecular insights into a therapeutic window of opportunity following traumatic stress exposure.Translational psychiatry · 2025Article
- The Role of the Glucocorticoid Receptor and Its Phosphorylation in Neurological Disorders.International journal of molecular sciences · 2025Review
- Single Intranasal Administration of Ucn3 Affects the Development of PTSD Symptoms in an Animal Model.International journal of molecular sciences · 2024Article
- Basal forebrain cholinergic systems as circuits through which traumatic stress disrupts emotional memory regulation.Neuroscience and biobehavioral reviews · 2024Review
- Neural Correlates and Molecular Mechanisms of Memory and Learning.International journal of molecular sciences · 2024Article
- Chronic adolescent stress alters GR-FKBP5 interactions in the hippocampus of adult female rats.Stress (Amsterdam, Netherlands) · 2024Article
- Glucocorticoids modulate neural activity via a rapid non-genomic effect on Kv2.2 channels in the central nervous system.Neurobiology of stress · 2024Article
- Effects of a True Prophylactic Treatment on Hippocampal and Amygdala Synaptic Plasticity and Gene Expression in a Rodent Chronic Stress Model of Social Defeat.International journal of molecular sciences · 2023Article
- Locked Out: Phoenixin-14 Does Not Cross a Stem-Cell-Derived Blood-Brain Barrier Model.Brain sciences · 2023Article
- The role of estrogen receptor manipulation during traumatic stress on changes in emotional memory induced by traumatic stress.Psychopharmacology · 2023Article
- Neuropharmacological Modulation of N-methyl-D-aspartate, Noradrenaline and Endocannabinoid Receptors in Fear Extinction Learning: Synaptic Transmission and Plasticity.International journal of molecular sciences · 2023Review
- Diosgenin normalization of disrupted behavioral and central neurochemical activity after single prolonged stress.Frontiers in pharmacology · 2023Article
- Review
- Pharmacological Implications of Adjusting Abnormal Fear Memory: Towards the Treatment of Post-Traumatic Stress Disorder.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Editorial of Special Issue 'Dissecting Neurological and Neuropsychiatric Diseases: Neurodegeneration and Neuroprotection'.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Central glucocorticoid receptor (GR) activity is enhanced following traumatic events, playing a key role in the stress-related cognitive abnormalities of posttraumatic stress disorder (PTSD). GR antagonists are expected to have potential as pharmacological agents to treat PTSD-related symptoms such as anxiety and fear memory disruption. However, an incubation period is usually required and stress-induced abnormalities do not develop immediately following the trauma; thus, the optimal intervention timing should be considered. Single prolonged stress (SPS) was employed as a rodent PTSD model to examine the effects of early or late (1-7 versus 8-14 days after the SPS) sub-chronic RU486 (a GR antagonist) administration. Behaviorally, fear conditioning and anxiety behavior were assessed using the fear-conditioning test and elevated T-maze (ETM), respectively. Neurochemically, the expressions of GR, FK506-binding proteins 4 and 5 (FKBP4 and FKBP5), and early growth response-1 (Egr-1) were assessed in the hippocampus, medial prefrontal cortex (mPFC), amygdala, and hypothalamus, together with the level of plasma corticosterone. Early RU486 administration could inhibit SPS-induced behavioral abnormalities and glucocorticoid system dysregulation by reversing the SPS-induced fear extinction deficit, and preventing SPS-reduced plasma corticosterone levels and SPS-induced Egr-1 overexpression in the hippocampus. Early RU486 administration following SPS also increased the FKBP5 level in the hippocampus and hypothalamus. Finally, both early and late RU486 administration inhibited the elevated hippocampal FKBP4 level and hypothalamus GR level in the SPS rats. Early intervention with a GR antagonist aids in the correction of traumatic stress-induced fear and anxiety dysregulation.
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