{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T12:49:35Z","timestamp":1782305375661,"version":"3.54.5"},"reference-count":147,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T00:00:00Z","timestamp":1781049600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T00:00:00Z","timestamp":1781049600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004281","name":"Narodowe Centrum Nauki","doi-asserted-by":"publisher","award":["2020\/39\/B\/NZ5\/01962"],"award-info":[{"award-number":["2020\/39\/B\/NZ5\/01962"]}],"id":[{"id":"10.13039\/501100004281","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Physiologica"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Excessive extracellular accumulation of K\n                    <jats:sup>+<\/jats:sup>\n                    plays a key role in the induction and propagation of seizures associated with temporal lobe epilepsy (TLE), and astrocytes are largely responsible for K\n                    <jats:sup>+<\/jats:sup>\n                    clearance from the extracellular space. Here, we review the TLE\u2010related changes in the content and\/or activity of proteins contributing to K\n                    <jats:sup>+<\/jats:sup>\n                    transport across the astrocytic cell membranes. Seizures, whether genetic or acquired, are linked with decreased expression and\/or mislocalization of the two key astroglia\u2010specific drivers of K\n                    <jats:sup>+<\/jats:sup>\n                    uptake: the inward rectifying potassium channel K\n                    <jats:sub>ir<\/jats:sub>\n                    4.1 and its spatial and functional partner, the water channel aquaporin 4 (AQP4). Among neural cells of the CNS, the high K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010responsive \u03b12 isoform of Na\n                    <jats:sup>+<\/jats:sup>\n                    \/K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010ATPase is specific for astrocytes and is substantially inactivated in the brains of TLE patients and experimental animals, albeit not always in epilepsies with a genetic background. The above data consistently support the involvement of malfunctional astrocytic K\n                    <jats:sup>+<\/jats:sup>\n                    transport as a factor facilitating seizures. By contrast, complex and variable, region\u2010dependent dynamics of the two\u2010pore domain potassium channels (K2P; TWIK, TASK, and TREK) were observed in astrocytes in the hippocampus, rendering their contribution to seizures difficult to interpret. Anti\u2010seizure medication targeting metabolic processes not directly related to astrocytic K\n                    <jats:sup>+<\/jats:sup>\n                    transport often reversed the unfavorably changed status of the astrocytic mediators of K\n                    <jats:sup>+<\/jats:sup>\n                    buffering.\n                  <\/jats:p>","DOI":"10.1111\/apha.70263","type":"journal-article","created":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T13:31:59Z","timestamp":1781098319000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Aberrant Potassium Handling by Astrocytes and Epileptic Seizures: A Synthetic Update"],"prefix":"10.1111","volume":"242","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6063-6228","authenticated-orcid":false,"given":"Jan","family":"Albrecht","sequence":"first","affiliation":[{"name":"Department of Neurotoxicology Mossakowski Medical Research Institute, Polish Academy of Sciences  Warsaw Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2879-9945","authenticated-orcid":false,"given":"Stanis\u0142aw J.","family":"Czuczwar","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology Medical University of Lublin  Lublin Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9640-2159","authenticated-orcid":false,"given":"W\u0142adys\u0142aw","family":"Laso\u0144","sequence":"additional","affiliation":[{"name":"Department of Experimental Neuroendocrinology Maj Institute of Pharmacology, Polish Academy of Sciences  Krak\u00f3w Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2592-9898","authenticated-orcid":false,"given":"Alexei","family":"Verkhratsky","sequence":"additional","affiliation":[{"name":"Faculty of Biology, Medicine and Health The University of Manchester  Manchester UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7388-3092","authenticated-orcid":false,"given":"Magdalena","family":"Zieli\u0144ska","sequence":"additional","affiliation":[{"name":"Department of Neurotoxicology Mossakowski Medical Research Institute, Polish Academy of Sciences  Warsaw Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,6,10]]},"reference":[{"key":"e_1_2_9_2_1","volume-title":"Neuroglia: Function and Pathology","author":"Verkhratsky 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