ArticleJournal of neurotrauma2013
Restoration of neuroendocrine stress response by glucocorticoid receptor or GABA(A) receptor antagonists after experimental traumatic brain injury.
Article in Journal of neurotrauma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Extracranial Effects of Traumatic Brain Injury: A Narrative Review.Clinics and practice · 2025Review
- Context is key: glucocorticoid receptor and corticosteroid therapeutics in outcomes after traumatic brain injury.Frontiers in cellular neuroscience · 2024Review
- Sleep fragmentation engages stress-responsive circuitry, enhances inflammation and compromises hippocampal function following traumatic brain injury.Experimental neurology · 2022Article
- Brain Trauma, Glucocorticoids and Neuroinflammation: Dangerous Liaisons for the Hippocampus.Biomedicines · 2022Review
- Temporal profile of serum metabolites and inflammation following closed head injury in rats is associated with HPA axis hyperactivity.Metabolomics : Official journal of the Metabolomic Society · 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
- Sex-Dependent Pathology in the HPA Axis at a Sub-acute Period After Experimental Traumatic Brain Injury.Frontiers in neurology · 2020Article
- Pituitary pathology in traumatic brain injury: a review.Pituitary · 2019Review
- Pre-treatment with microRNA-181a Antagomir Prevents Loss of Parvalbumin Expression and Preserves Novel Object Recognition Following Mild Traumatic Brain Injury.Neuromolecular medicine · 2019Article
- Stress reactivity after traumatic brain injury: implications for comorbid post-traumatic stress disorder.Behavioural pharmacology · 2019Review
- A case of methylprednisolone treatment for metronidazole-induced encephalopathy.BMC neurology · 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
- Neuroendocrine Abnormalities Following Traumatic Brain Injury: An Important Contributor to Neuropsychiatric Sequelae.Frontiers in endocrinology · 2018Review
- Assessment of the role of intracranial hypertension and stress on hippocampal cell apoptosis and hypothalamic-pituitary dysfunction after TBI.Scientific reports · 2017Article
- Brain and Serum Androsterone Is Elevated in Response to Stress in Rats with Mild Traumatic Brain Injury.Frontiers in neuroscience · 2016Article
- Traumatic brain injury induces neuroinflammation and neuronal degeneration that is associated with escalated alcohol self-administration in rats.Behavioural brain research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that traumatic brain injury (TBI) produced by moderate controlled cortical impact (CCI) attenuates the stress response of the hypothalamic-pituitary-adrenal (HPA) axis between 21 and 70 days postinjury and enhances the sensitivity of the stress response to glucocorticoid negative feedback. In the current study, we investigated two possible mechanisms for the CCI-induced attenuation of the HPA stress response-i.e, glucocorticoid receptor (GR) and GABA-mediated inhibition of the HPA axis, with the GR antagonist, mifepristone (RU486), or the GABA(A)-receptor antagonist, bicuculline. In addition, we examined the effect of moderate CCI on GR and inhibitory neurons histologically in subfields of the hippocampus, medial prefrontal cortex, and amygdala. We show that at 30-min after onset of restraint stress, GR as well as GABA antagonism with MIFE or BIC, respectively, reversed the attenuating effects of moderate CCI on the stress-induced HPA response. Our histological results demonstrate that moderate CCI led to a loss of glutamic acid decarboxylase 67 or parvalbumin-positive inhibitory neurons within regions of the hippocampus and amygdala but did not lead to significant increases in GR in these regions. These findings indicate that suppression of the stress-induced HPA response after moderate CCI is mediated by the inhibitory actions of both GR and GABA, with a corresponding loss of inhibitory neurons within brain regions with neural pathways affecting limbic stress-integrative pathways.
Indexed as
Identifiers
What OpenQuestion holds
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.