{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T12:33:58Z","timestamp":1789216438381,"version":"build-2803163510"},"reference-count":42,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T00:00:00Z","timestamp":1097193600000},"content-version":"vor","delay-in-days":3933,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[1994,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The possible antigenicity of synaptotagmin, a synaptic vesicle protein acting as a cooperative calcium (Ca<jats:sup>2+<\/jats:sup>) receptor in exocytosis, was tested to determine whether it is involved in the induction of Lambert\u2010Eaton myasthenic syndrome in which antibodies against voltage\u2010dependent Ca<jats:sup>2+<\/jats:sup> channels or related molecules play a pathogenic role. Repeated injections to Lewis rats with peptides of synaptotagmin residues 20 through 53 or 1 through 30 that are presumably exposed at the nerve terminal surface during exocytosis induced corresponding antipeptide antibodies; on immunoblots, antibodies recognized synaptotagmin that was expressed in the clonal cells. Electrophysiologically, the peptide (residues 20\u201353)\u2010immunized rats showed (1) reduced acetylcholine quantal content of end\u2010plate potential, (2) an increase in quantal content at high extracellular Ca<jats:sup>2+<\/jats:sup> concentration, and (3) early facilitation followed by less marked depression of end\u2010plate potential amplitude at a tetanic rate of repetitive nerve stimulation. Findings are similar to those in human Lambert\u2010Eaton myasthenic syndrome and passively transferred Lambert\u2010Eaton myasthenic syndrome in mice, and thus suggest that antibody to a synaptotagmin\u2013voltage\u2010dependent Ca<jats:sup>2+<\/jats:sup> channel complex may be involved in the pathogenesis of Lambert\u2010Eaton myasthenic syndrome. The peptide (residues 1\u201330)\u2010immunized rats showed no electrophysiological abnormality.<\/jats:p>","DOI":"10.1002\/ana.410350112","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T15:58:25Z","timestamp":1104595105000},"page":"74-80","source":"Crossref","is-referenced-by-count":48,"title":["Synaptotagmin can cause an immune\u2010mediated model of Lambert\u2010Eaton myasthenic syndrome in 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