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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2026,5,26]]},"abstract":"<jats:p>\n                    Autoantibodies against leucine-rich glioma inactivated 1 protein (LGI1) lead to limbic encephalitis, a rare neurological autoimmune disorder characterized by faciobrachial dystonic seizures and memory deficits. While animal models provide precious insights into the mechanisms of LGI1 autoantibody action, species-specific confirmation is lacking. In this study, we investigated the effects of patient-derived LGI1 monoclonal antibodies (LGI1 mAb) on CA3 pyramidal neurons using cultured ex vivo human hippocampal slices, providing a unique platform to study disease mechanisms in a homologous, clinically relevant context. Under incubation conditions, human CA3 neurons preserved their morphology, were intrinsically excitable and received spontaneous excitatory currents with large amplitudes and frequencies suggestive of \u201cgiant\u201d AMPA receptor-mediated currents. In slices exposed to LGI1 mAb, human CA3 pyramidal neurons displayed increased action potential (AP) firing frequency, mirroring the effects observed with the K\n                    <jats:sub>v<\/jats:sub>\n                    1.1 channel blocker dendrotoxin-K (DTX-K). This increase likely resulted from a decreased K\n                    <jats:sub>v<\/jats:sub>\n                    1.1 channel activity at the axonal initial segment, as indicated by alterations in AP properties, including spike latency at rheobase and depolarizing ramp slope. Differences between LGI1 mAb and DTX-K effects on some AP properties suggested distinct mechanisms of action and emphasized the need for further exploration of downstream pathways. Our findings underscore the importance of species-specific confirmatory studies of disease mechanisms and give insight into possibilities and limitations of human hippocampal slice cultures as a translational model for the investigation of disease mechanisms beyond epilepsy, including the effects of pharmacological compounds and autoantibodies.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2510121123","type":"journal-article","created":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T19:11:12Z","timestamp":1779131472000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":1,"title":["The functional impact of LGI1 autoantibodies on human CA3 pyramidal neurons"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9513-6378","authenticated-orcid":false,"given":"Laura","family":"Monni","sequence":"first","affiliation":[{"name":"Department of Neurology and Experimental Neurology, 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