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In TLE, recurrent mossy fiber sprouting from dentate gyrus granule cells (DGCs) crea an aberrant epileptogenic network between DGCs which operates via ectopically expressed GluK2\/GluK5\u2010containing kainate receptors (KARs). TLE patients are often resistant to anti\u2010seizure medications and suffer significant comorbidities; hence, there is an urgent need for novel therapies. Previously, we have shown that GluK2 knockout mice are protected from seizures. This study aims at providing evidence that downregulating KARs in the hippocampus using gene therapy reduces chronic epileptic discharges in TLE.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We combined molecular biology and electrophysiology in rodent models of TLE and in hippocampal slices surgically resected from patients with drug\u2010resistant TLE.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Here, we confirmed the translational potential of KAR suppression using a non\u2010selective KAR antagonist that markedly attenuated interictal\u2010like epileptiform discharges (IEDs) in TLE patient\u2010derived hippocampal slices. An adeno\u2010associated virus (AAV) serotype\u20109 vector expressing anti\u2010\n                      <jats:italic>grik2<\/jats:italic>\n                      miRNA was engineered to specifically downregulate GluK2 expression. Direct delivery of AAV9\u2010anti\n                      <jats:italic>grik2<\/jats:italic>\n                      miRNA into the hippocampus of TLE mice led to a marked reduction in seizure activity. Transduction of TLE patient hippocampal slices reduced levels of GluK2 protein and, most importantly, significantly reduced IEDs.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>Our gene silencing strategy to knock down aberrant GluK2 expression demonstrates inhibition of chronic seizure in a mouse TLE model and IEDs in cultured slices derived from TLE patients. These results provide proof\u2010of\u2010concept for a gene therapy approach targeting GluK2 KARs for drug\u2010resistant TLE patients. ANN NEUROL 2023;94:745\u2013761<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.26723","type":"journal-article","created":{"date-parts":[[2023,6,21]],"date-time":"2023-06-21T10:13:52Z","timestamp":1687342432000},"page":"745-761","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["<scp>GluK2<\/scp>\n                    Is a Target for Gene Therapy in Drug\u2010Resistant Temporal Lobe Epilepsy"],"prefix":"10.1002","volume":"94","author":[{"given":"C\u00e9line","family":"Boileau","sequence":"first","affiliation":[{"name":"Aix\u2010Marseille Univ. INSERM  Marseille France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Severine","family":"Deforges","sequence":"additional","affiliation":[{"name":"Univ. 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