{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T07:13:54Z","timestamp":1789370034607,"version":"build-2803163510"},"reference-count":41,"publisher":"National Academy of Sciences","issue":"7","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2008,2,19]]},"abstract":"<jats:p>\n                    Voltage-gated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channels (VGCCs) are membrane proteins that determine the activity and survival of neurons, and mutations in the P\/Q-type VGCCs are known to cause cerebellar ataxia. VGCC dysfunction may also underlie acquired peripheral and central nervous system diseases associated with small-cell lung cancer, including Lambert\u2013Eaton myasthenic syndrome (LEMS) and paraneoplastic cerebellar ataxia (PCA). The pathogenic role of anti-VGCC antibody in LEMS is well established. Although anti-VGCC antibody is also found in a significant fraction of PCA patients, its contribution to PCA is unclear. Using a polyclonal peptide antibody against a major immunogenic region in P\/Q-type VGCCs (the extracellular Domain-III S5\u2013S6 loop), we demonstrated that such antibody was sufficient to inhibit VGCC function in neuronal and recombinant VGCCs, alter cerebellar synaptic transmission, and confer the phenotype of cerebellar ataxia. Our data support the hypothesis that anti-VGCC antibody may play a significant role in the pathogenesis of cerebellar dysfunction in PCA.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0710771105","type":"journal-article","created":{"date-parts":[[2008,2,13]],"date-time":"2008-02-13T20:59:16Z","timestamp":1202936356000},"page":"2705-2710","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":51,"title":["Anti-Ca\n                    <sup>2+<\/sup>\n                    channel antibody attenuates Ca\n                    <sup>2+<\/sup>\n                    currents and mimics cerebellar ataxia\n                    <i>in vivo<\/i>"],"prefix":"10.1073","volume":"105","author":[{"given":"Yaping Joyce","family":"Liao","sequence":"first","affiliation":[{"name":"Departments of *Molecular and Cellular Physiology,"},{"name":"Ophthalmology and Neurology, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Parsa","family":"Safa","sequence":"additional","affiliation":[{"name":"Departments of *Molecular and Cellular Physiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi-Ren","family":"Chen","sequence":"additional","affiliation":[{"name":"Departments of *Molecular and Cellular Physiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raymond A.","family":"Sobel","sequence":"additional","affiliation":[{"name":"Pathology, Stanford University School of Medicine, Stanford, CA 94305"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward S.","family":"Boyden","sequence":"additional","affiliation":[{"name":"Departments of *Molecular and Cellular Physiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard W.","family":"Tsien","sequence":"additional","affiliation":[{"name":"Departments of *Molecular and Cellular Physiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2008,2,19]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1957.02970480021005"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.23.7.764"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1164\/ajrccm\/147.5.1229"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199506013322203"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00194096"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra023009"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.neuro.22.1.175"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410400510"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(89)90109-4"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1750-3639.1999.tb00226.x"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.16.7076"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/0896-6273(95)90155-8"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.10497"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/120.8.1279"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jneuroim.2005.04.001"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.59.5.764"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.42.10.1944"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.10392"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.14.8328"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.15-04-02995.1995"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.20028560"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.15-01-00274.1995"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1998.tb11004.x"},{"key":"e_1_3_3_24_2","first-page":"S17","article-title":"Lambert\u2013Eaton myasthenic syndrome: Electrophysiological evidence for a humoral factor.","volume":"5","author":"Newsom-Davis J","year":"1982","unstructured":"J Newsom-Davis, et al., Lambert\u2013Eaton myasthenic syndrome: Electrophysiological evidence for a humoral factor. 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