Calcium channel peptide can cause an autoimmune-mediated model of Lambert-Eaton myasthenic syndrome in rats

Citation
K. Komai et al., Calcium channel peptide can cause an autoimmune-mediated model of Lambert-Eaton myasthenic syndrome in rats, J NEUR SCI, 166(2), 1999, pp. 126-130
Citations number
21
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF THE NEUROLOGICAL SCIENCES
ISSN journal
0022-510X → ACNP
Volume
166
Issue
2
Year of publication
1999
Pages
126 - 130
Database
ISI
SICI code
0022-510X(19990701)166:2<126:CCPCCA>2.0.ZU;2-1
Abstract
The Lambert-Eaton myasthenic syndrome (LEMS) is a disorder of neuromuscular transmission characterized by the reduced quantal release of acetylcholine from the motor nerve terminal, wherein the P/Q-type of voltage-gated calci um channel (VGCC) and is attacked by a majority of LEMS antibodies. Using t he molecular structure of the alpha 1 subunit (consisting of 4 domains) of the P/Q-type VGCC as a reference, we synthesized the extracellular region ( S5-S6 link;er) of the domain III, known as the segment which plays an impor tant role in channel functions. Six of the ten Lewis rats immunized with th is synthetic peptide conjugated with carrier protein showed moderate weakne ss (grade 1 in a 3-graded scale, for myasthenic weakness in experimental an imals) and a reduction in acetylcholine quantum content of end-plate potent ials. Antipeptide antibodies raised in test rats reacted with omega-conotox in MVIIC-sensitive cerebellar extract (P/Q-type VGCC) and the domain III pe ptide inhibited the binding of rat antibodies to VGCCs. Our findings sugges t the identification of one of the potential epitopes of LEMS antibodies. ( C) 1999 Elsevier Science B.V. All rights reserved.