{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Alves M"],"funding":["NINDS NIH HHS"],"pagination":["110599"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12348367"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["278"],"pubmed_abstract":["Traumatic brain injury (TBI) is a leading cause of acquired epilepsy, with post-traumatic epilepsy (PTE) significantly contributing to morbidity and mortality. To date, there is no treatment capable to prevent the development of PTE, which remains an urgent unmet need. Previous studies suggest that adenosine A<sub>2A</sub> receptor (A<sub>2A</sub>R) activation and glutamate transporter 1 (GLT-1) dysregulation may contribute to epileptogenesis, however, it is unclear whether therapeutic targeting of the A<sub>2A</sub>R or GLT-1 can attenuate TBI-induced hyperexcitability, and whether there are synergistic interactions between the two. Here, we investigated the therapeutic potential of two FDA approved drugs istradefylline (A<sub>2A</sub>R inhibitor) and ceftriaxone (GLT-1 activator) in prev"],"journal":["Neuropharmacology"],"pubmed_title":["Adenosine A&lt;sub&gt;2A&lt;/sub&gt; receptor and glial glutamate transporter GLT-1 are synergistic targets to reduce brain hyperexcitability after traumatic brain injury in mice."],"pmcid":["PMC12348367"],"funding_grant_id":["R01 NS127846"],"pubmed_authors":["Fedele D","Kalmeijer R","Engel T","Alves M","Gerbatin R","Boison D"],"additional_accession":[]},"is_claimable":false,"name":"Adenosine A&lt;sub&gt;2A&lt;/sub&gt; receptor and glial glutamate transporter GLT-1 are synergistic targets to reduce brain hyperexcitability after traumatic brain injury in mice.","description":"Traumatic brain injury (TBI) is a leading cause of acquired epilepsy, with post-traumatic epilepsy (PTE) significantly contributing to morbidity and mortality. To date, there is no treatment capable to prevent the development of PTE, which remains an urgent unmet need. Previous studies suggest that adenosine A<sub>2A</sub> receptor (A<sub>2A</sub>R) activation and glutamate transporter 1 (GLT-1) dysregulation may contribute to epileptogenesis, however, it is unclear whether therapeutic targeting of the A<sub>2A</sub>R or GLT-1 can attenuate TBI-induced hyperexcitability, and whether there are synergistic interactions between the two. Here, we investigated the therapeutic potential of two FDA approved drugs istradefylline (A<sub>2A</sub>R inhibitor) and ceftriaxone (GLT-1 activator) in prev","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-05-01T21:04:22.69Z","creation":"2026-04-07T17:16:07.722Z"},"accession":"S-EPMC12348367","cross_references":{"pubmed":["40712754"],"doi":["10.1016/j.neuropharm.2025.110599"]}}