ArticleJournal of neurotrauma2013
Ceftriaxone treatment after traumatic brain injury restores expression of the glutamate transporter, GLT-1, reduces regional gliosis, and reduces post-traumatic seizures in the rat.
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 104 papers, 1 of them a synthesis that pooled it.
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Who cites it
104 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Early post-traumatic seizure as severity predictor of traumatic brain injury: A meta-analysis and systematic review.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026Pooled it
- cGAS-mediated type I IFN signaling contributes to disease progression in drug-refractory epilepsy.Nature neuroscience · 2026Article
- Review
- cGAS-mediated IFN-I signaling contributes to disease progression in drug-refractory epilepsy.bioRxiv : the preprint server for biology · 2026Article
- The NMDAR/TRPM4 death complex is a major promoter of disease progression in the 5xFAD mouse model of Alzheimer's disease.Molecular psychiatry · 2026Article
- Infant traumatic brain injury with a biphasic clinical course and late diffusion restriction: a case report.Frontiers in neuroscience · 2026Article
- Neuroprotective effects of ceftriaxone after severe traumatic brain injury in male rats: a behavioral, biochemical, and histological study.Annals of medicine and surgery (2012) · 2026Article
- Adenosine ANeuropharmacology · 2025Article
- Upregulation of GLT-1 Expression Attenuates Neuronal Apoptosis and Cognitive Dysfunction via Inhibiting the CB1-CREB Signaling Pathway in Mice with Traumatic Brain Injury.Biomolecules · 2025Article
- Advances and challenges in experimental models of posttraumatic epilepsy for therapeutic interventions.Pharmacological reviews · 2025Review
- Role of astrocytes in the pathogenesis of perinatal brain injury.Molecular medicine (Cambridge, Mass.) · 2025Review
- Cellular and molecular mechanisms of pathological tau phosphorylation in traumatic brain injury: implications for chronic traumatic encephalopathy.Molecular neurodegeneration · 2025Review
- Glutamate uptake is transiently compromised in the perilesional cortex following controlled cortical impact.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Enhancement of Glutamate Uptake as Novel Antiseizure Approach: Preclinical Proof of Concept.Annals of neurology · 2025Article
- Peripheral nerve injury recovery enhanced by ceftriaxone: a preclinical investigation.Acta cirurgica brasileira · 2025Article
- New epilepsy therapies in development.Nature reviews. Drug discovery · 2024Review
- Neuroprotective effects of naltrexone in a mouse model of post-traumatic seizures.Scientific reports · 2024Article
- Current state of neuroprotective therapy using antibiotics in human traumatic brain injury and animal models.BMC neuroscience · 2024Review
- Depressed glutamate transporter 1 expression in a mouse model of Dravet syndrome.Annals of clinical and translational neurology · 2023Article
- Neuropharmacological insight into preventive intervention in posttraumatic epilepsy based on regulating glutamate homeostasis.CNS neuroscience & therapeutics · 2023Review
44 more citing papers are in PubMed but not listed here.
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6 authors.
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Abstract
Excessive extracellular glutamate after traumatic brain injury (TBI) contributes to excitotoxic cell death and likely to post-traumatic epilepsy. Glutamate transport is the only known mechanism of extracellular glutamate clearance, and glutamate transporter 1 (GLT-1) is the major glutamate transporter of the mammalian brain. We tested, by immunoblot, in the rat lateral fluid percussion injury TBI model whether GLT-1 expression is depressed in the cortex after TBI, and whether GLT-1 expression after TBI is restored after treatment with ceftriaxone, a well-tolerated β-lactam antibiotic previously shown to enhance GLT-1 expression in noninjured animals. We then tested whether treatment with ceftriaxone mitigates the associated regional astrogliosis, as reflected by glial fibrillary acid protein (GFAP) expression, and also whether ceftriaxone treatment mitigates the severity of post-traumatic epilepsy. We found that 7 days after TBI, GLT-1 expression in the ipsilesional cortex was reduced by 29% (n=7/group; p<0.01), relative to the contralesional cortex. However, the loss of GLT-1 expression was reversed by treatment with ceftriaxone (200 mg/kg, daily, intraperitoneally). We found that ceftriaxone treatment also decreased the level of regional GFAP expression by 43% in the lesioned cortex, relative to control treatment with saline (n=7 per group; p<0.05), and, 12 weeks after injury, reduced cumulative post-traumatic seizure duration (n=6 rats in the ceftriaxone treatment group and n=5 rats in the saline control group; p<0.001). We cautiously conclude that our data suggest a potential role for ceftriaxone in treatment of epileptogenic TBI.
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