ArticleExperimental neurology2015
JAK/STAT pathway regulation of GABAA receptor expression after differing severities of experimental TBI.
Article in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 69 citations in OpenAlex.
- Article
- Potential Protective Effects of Naloxone in Traumatic Brain Injury Through JAK2/STAT3 Signaling Modulation.Life (Basel, Switzerland) · 2026Article
- Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026Review
- Advances and challenges in experimental models of posttraumatic epilepsy for therapeutic interventions.Pharmacological reviews · 2025Review
- Functional Alterations in Parvalbumin-Positive Interneurons after Traumatic Brain Injury in Somatosensory Cortex of Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Disease modification upon 2 weeks of tofacitinib treatment in a mouse model of chronic epilepsy.Science translational medicine · 2025Article
- Ruxolitinib-dependent reduction of seizure load and duration is accompanied by spatial memory improvement in the rat pilocarpine model of temporal lobe epilepsy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Deep postnatal phenotyping of a new mouse model of nonketotic hyperglycinemia.Journal of inherited metabolic disease · 2024Article
- Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury.Heliyon · 2024Review
- Inhibition of Neuron-Restrictive Silencing Factor (REST/NRSF) Chromatin Binding Attenuates Epileptogenesis.eNeuro · 2024Article
- Implications of Iron in Ferroptosis, Necroptosis, and Pyroptosis as Potential Players in TBI Morbidity and Mortality.ASN neuro · 2024Review
- Diet composition and sterilization modifies intestinal microbiome diversity and burden of Theiler's virus infection-induced acute seizures.bioRxiv : the preprint server for biology · 2023Article
- Janus kinase inhibitors are potential therapeutics for amyotrophic lateral sclerosis.Translational neurodegeneration · 2023Review
- Interleukin 6 (IL-6) Regulates GABAA Receptors in the Dorsomedial Hypothalamus Nucleus (DMH) through Activation of the JAK/STAT Pathway to Affect Heart Rate Variability in Stressed Rats.International journal of molecular sciences · 2023Article
- Cellular and Molecular Pathophysiology of Traumatic Brain Injury: What Have We Learned So Far?Biology · 2023Review
- Inhibition of the JAK/STAT Pathway With Baricitinib Reduces the Multiple Organ Dysfunction Caused by Hemorrhagic Shock in Rats.Annals of surgery · 2023Article
- Neuroimmune interactions with binge alcohol drinking in the cerebellum of IL-6 transgenic mice.Neuropharmacology · 2023Article
- Cannabidiol reveals a disruptive strategy for 21st century epilepsy drug discovery.Experimental neurology · 2023Review
- Cannabidiol's neuroprotective properties and potential treatment of traumatic brain injuries.Frontiers in neurology · 2023Review
- Zolpidem Profoundly Augments Spared Tonic GABAFrontiers in systems neuroscience · 2022Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Synaptic inhibition in the adult brain is primarily mediated by the γ-aminobutyric acid (GABA) type A receptor (GABA(A)R). The distribution, properties, and dynamics of these receptors are largely determined by their subunit composition. Alteration of subunit composition after a traumatic brain injury (TBI) may result in abnormal increased synaptic firing and possibly contribute to injury-related pathology. Several studies have shown that the Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) signaling pathway can alter GABA(A)R subunit expression. The present study investigated changes in JAK/STAT pathway activation after two different severities of experimental TBI in the mouse using the controlled cortical impact (CCI) model. It also investigated whether modulating the activation of the JAK/STAT pathway after severe controlled cortical impact (CCI-S) with a JAK/STAT inhibitor (WP1066) alters post-traumatic epilepsy development and/or neurological recovery after injury. Our results demonstrated differential changes in both the activation of STAT3 and the expression of the GABA(A)R α1 and γ2 subunit levels that were dependent on the severity of the injury. The change in the GABA(A)R α1 subunit levels appeared to be at least partly transcriptionally mediated. We were able to selectively reverse the decrease in GABA(A)R α1 protein levels with WP1066 treatment after CCI injury. WP1066 treatment also improved the degree of recovery of vestibular motor function after injury. These findings suggest that the magnitude of JAK/STAT pathway activation and GABA(A)R α1 subunit level decrease is dependent on injury severity in this mouse model of TBI. In addition, reducing JAK/STAT pathway activation after severe experimental TBI reverses the decrease in the GABA(A)R α1 protein levels and improves vestibular motor recovery.
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