ArticleJournal of biomedical science2010
Traumatic brain injury and the effects of diazepam, diltiazem, and MK-801 on GABA-A receptor subunit expression in rat hippocampus.
Article in Journal of biomedical science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 52 citations in OpenAlex.
- TNF-α in traumatic brain injury: a bidirectional effect in regulating neuroimmune and inflammatory responses.Cellular and molecular life sciences : CMLS · 2025Review
- Are GABAergic drugs beneficial in providing neuroprotection after traumatic brain injuries? A comprehensive literature review of preclinical studies.Frontiers in neurology · 2023Review
- Repetitive mild traumatic brain injury induces persistent alterations in spontaneous synaptic activity of hippocampal CA1 pyramidal neurons.IBRO neuroscience reports · 2022Article
- Article
- The Emerging Roles of π Subunit-Containing GABAInternational journal of medical sciences · 2021Review
- Challenges of Delirium Management in Patients with Traumatic Brain Injury: From Pathophysiology to Clinical Practice.Current neuropharmacology · 2021Review
- Sigma-1 Receptor: A Potential Therapeutic Target for Traumatic Brain Injury.Frontiers in cellular neuroscience · 2021Review
- Exploring Neuronal Vulnerability to Head Trauma Using a Whole Exome Approach.Journal of neurotrauma · 2020Article
- Low Prefrontal GABA Levels Are Associated With Poor Cognitive Functions in Professional Boxers.Frontiers in human neuroscience · 2019Article
- Spontaneous recovery of traumatic brain injury-induced functional deficits is not hindered by daily administration of lorazepam.Behavioural brain research · 2018Article
- Primary Blast-Induced Changes in Akt and GSKFrontiers in neurology · 2017Article
- Septohippocampal Neuromodulation Improves Cognition after Traumatic Brain Injury.Journal of neurotrauma · 2015Article
- Protective effect of a calcium channel blocker "diltiazem" on aluminum chloride-induced dementia in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- JAK/STAT pathway regulation of GABAA receptor expression after differing severities of experimental TBI.Experimental neurology · 2015Article
- Glutamate and GABA imbalance following traumatic brain injury.Current neurology and neuroscience reports · 2015Review
- Expression of GABA receptor subunits in the hippocampus and thalamus after experimental traumatic brain injury.Neuropharmacology · 2015Article
- Biomarkers of cognitive dysfunction in traumatic brain injury.Journal of neural transmission (Vienna, Austria : 1996) · 2014Review
- Neurosteroid interactions with synaptic and extrasynaptic GABA(A) receptors: regulation of subunit plasticity, phasic and tonic inhibition, and neuronal network excitability.Psychopharmacology · 2013Review
- Restoration of neuroendocrine stress response by glucocorticoid receptor or GABA(A) receptor antagonists after experimental traumatic brain injury.Journal of neurotrauma · 2013Article
- Exendin-4, a glucagon-like peptide-1 receptor agonist prevents mTBI-induced changes in hippocampus gene expression and memory deficits in mice.Experimental neurology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundExcitatory amino acid release and subsequent biochemical cascades following traumatic brain injury (TBI) have been well documented, especially glutamate-related excitotoxicity. The effects of TBI on the essential functions of inhibitory GABA-A receptors, however, are poorly understood.
methodsWe used Western blot procedures to test whether in vivo TBI in rat altered the protein expression of hippocampal GABA-A receptor subunits alpha1, alpha2, alpha3, alpha5, beta3, and gamma2 at 3 h, 6 h, 24 h, and 7 days post-injury. We then used pre-injury injections of MK-801 to block calcium influx through the NMDA receptor, diltiazem to block L-type voltage-gated calcium influx, or diazepam to enhance chloride conductance, and re-examined the protein expressions of alpha1, alpha2, alpha3, and gamma2, all of which were altered by TBI in the first study and all of which are important constituents in benzodiazepine-sensitive GABA-A receptors.
resultsWestern blot analysis revealed no injury-induced alterations in protein expression for GABA-A receptor alpha2 or alpha5 subunits at any time point post-injury. Significant time-dependent changes in alpha1, alpha3, beta3, and gamma2 protein expression. The pattern of alterations to GABA-A subunits was nearly identical after diltiazem and diazepam treatment, and MK-801 normalized expression of all subunits 24 hours post-TBI.
conclusionsThese studies are the first to demonstrate that GABA-A receptor subunit expression is altered by TBI in vivo, and these alterations may be driven by calcium-mediated cascades in hippocampal neurons. Changes in GABA-A receptors in the hippocampus after TBI may have far-reaching consequences considering their essential importance in maintaining inhibitory balance and their extensive impact on neuronal function.
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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.