ArticleNeuroscience2012
Effects of acute restraint-induced stress on glucocorticoid receptors and brain-derived neurotrophic factor after mild traumatic brain injury.
Article in Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Previous exposure to traumatic brain injury alters acute stress responses in mice.Scientific reports · 2025Article
- Characterization of GABAergic marker expression in prefrontal cortex in dexamethasone induced depression/anxiety model.Frontiers in endocrinology · 2024Article
- Deplete and repeat: microglial CSF1R inhibition and traumatic brain injury.Frontiers in cellular neuroscience · 2024Review
- The Neurobiological Links between Stress and Traumatic Brain Injury: A Review of Research to Date.International journal of molecular sciences · 2022Review
- Sleep fragmentation engages stress-responsive circuitry, enhances inflammation and compromises hippocampal function following traumatic brain injury.Experimental neurology · 2022Article
- Restraint Stress Delays the Recovery of Neurological Impairments and Exacerbates Brain Damages through Activating Endoplasmic Reticulum Stress-mediated Neurodegeneration/Autophagy/Apopotosis post Moderate Traumatic Brain Injury.Molecular neurobiology · 2022Article
- Neurobiological Links between Stress, Brain Injury, and Disease.Oxidative medicine and cellular longevity · 2022Review
- Acute Cortisol Profile Associations With Cognitive Impairment After Severe Traumatic Brain Injury.Neurorehabilitation and neural repair · 2021Article
- TBI Rehabilomics Research: Conceptualizing a humoral triad for designing effective rehabilitation interventions.Neuropharmacology · 2019Review
- Experimental Traumatic Brain Injury Induces Chronic Glutamatergic Dysfunction in Amygdala Circuitry Known to Regulate Anxiety-Like Behavior.Frontiers in neuroscience · 2019Article
- Factors promoting vulnerability to dysregulated stress reactivity and stress-related disease.Journal of neuroendocrinology · 2018Review
- Elucidating opportunities and pitfalls in the treatment of experimental traumatic brain injury to optimize and facilitate clinical translation.Neuroscience and biobehavioral reviews · 2018Review
- Central CRF2 receptor antagonism reduces anxiety states during amphetamine withdrawal.Neuroscience research · 2014Article
- Recovery of stress response coincides with responsiveness to voluntary exercise after traumatic brain injury.Journal of neurotrauma · 2014Article
- Temperature and heart rate responses to exercise following mild traumatic brain injury.Journal of neurotrauma · 2013Article
- Quality and timing of stressors differentially impact on brain plasticity and neuroendocrine-immune function in mice.Neural plasticity · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We have previously reported that experimental mild traumatic brain injury results in increased sensitivity to stressful events during the first post-injury weeks, as determined by analyzing the hypothalamic-pituitary-adrenal (HPA) axis regulation following restraint-induced stress. This is the same time period when rehabilitative exercise has proven to be ineffective after a mild fluid-percussion injury (FPI). Here we evaluated effects of stress on neuroplasticity. Adult male rats underwent either an FPI or sham injury. Additional rats were only exposed to anesthesia. Rats were exposed to 30 min of restraint stress, followed by tail vein blood collection at post-injury days (PID) 1, 7, and 14. The response to dexamethasone (DEX) was also evaluated. Hippocampal tissue was collected 120 min after stress onset. Brain-derived neurotrophic factor (BDNF) along with glucocorticoid (GR) and mineralocorticoid (MR) receptors was determined by Western blot analysis. Results indicated injury-dependent changes in glucocorticoid and mineralocorticoid receptors that were influenced by the presence of dexamethasone. Control and FPI rats responded differentially to DEX in that GR increases after receiving the lower dose of DEX were longer lasting in the FPI group. A suppression of MR was found at PID 1 in vehicle-treated FPI and Sham groups. Decreases in the precursor form of BDNF were observed in different FPI groups at PIDs 7 and 14. These findings suggest that the increased sensitivity to stressful events during the first post-injury weeks, after a mild FPI, has an impact on hippocampal neuroplasticity.
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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.