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In DRE, disruptions in GABA\n                    <jats:sub>A<\/jats:sub>\n                    receptors (GABA\n                    <jats:sub>A<\/jats:sub>\n                    R) function through altered subunit composition, receptor mislocalisation, or impaired trafficking, undermine inhibitory control and contribute to persistent seizures. The regulation of intracellular chloride by NKCC1 and KCC2 further shapes GABA\n                    <jats:sub>A<\/jats:sub>\n                    R-mediated inhibition, where imbalances in these transporters exacerbate network hyperexcitability. Structural studies, including high-resolution cryo-EM, reveal how ligand binding, receptor conformation, and interactions with auxiliary proteins modulate GABA\n                    <jats:sub>A<\/jats:sub>\n                    R activity, offering insights into why some subtypes respond differently to benzodiazepines or neurosteroids. Emerging evidence suggests that targeting receptor-associated proteins, trafficking pathways, or specific subunit combinations may offer novel ways to restore inhibitory tone and overcome pharmacoresistance. Understanding how these molecular, structural, and cellular factors converge to alter GABA\n                    <jats:sub>A<\/jats:sub>\n                    R function provides a roadmap for designing therapies that are both effective and precise, especially for DRE. By unravelling the mechanisms behind GABA\n                    <jats:sub>A<\/jats:sub>\n                    R dysfunction in DRE, new avenues open for restoring network stability and improving outcomes for patients living with DRE.\n                  <\/jats:p>","DOI":"10.1007\/s10571-026-01759-x","type":"journal-article","created":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T17:24:14Z","timestamp":1780593854000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["GABAA Receptors and Drug-Resistant Epilepsy: Why It\u2019s Time to Think Outside the Pore"],"prefix":"10.1007","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6579-3062","authenticated-orcid":false,"given":"Iman Imtiyaz Ahmed","family":"Juvale","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0993-5622","authenticated-orcid":false,"given":"Alina","family":"Arulsamy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,6,4]]},"reference":[{"key":"1759_CR1","doi-asserted-by":"publisher","first-page":"107014","DOI":"10.1016\/j.eplepsyres.2022.107014","volume":"186","author":"S Aboumatar","year":"2022","unstructured":"Aboumatar S, Biton V, Wechsler R, Ferrari L, Rosenfeld WE (2022) Post hoc analysis of a phase 3 study for treatment of uncontrolled focal seizures: Adjunctive cenobamate dose and seizure reduction by baseline seizure frequency. 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