Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1990-7-12
pubmed:abstractText
1. The effect of Lambert-Eaton myasthenic syndrome (LEMS) immunoglobulin G (IgG) on Ca2+ channels in undifferentiated mouse neuroblastoma x rat glioma hybrid cells (NG 108 15) was studied using the whole-cell patch clamp technique. 2. Sustained inward Ca2+ channel currents were evoked by depolarizing pulses from holding potentials of -80 and -40 mV, and were blocked by 5 microM-nitrendipine (L-type currents). Transient inward Ca2+ channel currents were activated from a holding potential of -80 mV by small depolarizing steps (T-type currents). Noradrenaline (10 microM) was without effect on transient currents. 3. LEMS IgG selectively reduced sustained (L-type) Ca2+ channel current amplitudes evoked from either holding potential used. In the presence of nitrendipine (5 microM), there was no significant effect of LEMS IgG on the remaining transient (T-type) Ca2+ channel current amplitudes. 4. Studies of the potential for maximal inward current indicated that voltage sensitivities of both L- and T-type Ca2+ channel current amplitudes were unaffected by LEMS IgG, whether recorded in the presence or absence of nitrendipine. LEMS IgG had no significant effect on the time-to-peak or decay of Ca2+ channel currents. 5. It is concluded that LEMS IgG acts selectively to cause functional loss of L-type, but not T-type, Ca2+ channels in NG 108 15 cells. Any effect of LEMS IgG on N-type channels (not present in these undifferentiated cells) was not studied here. LEMS IgG also acts at motor nerve terminal Ca2+ channels leading to muscle weakness. Thus antigenic similarities must exist between L-type channels in NG 108 15 cells and Ca2+ channels at motor nerve terminals.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-13339282, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2410796, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2414666, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2443646, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2447652, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2450991, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2451016, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2451017, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2469160, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2838124, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2907138, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-2992356, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-302922, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-316102, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-3392676, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-3479929, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-3662451, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-4330759, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-6111072, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-6114283, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-6270629, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-6584877, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161458-6655585
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-3751
pubmed:author
pubmed:issnType
Print
pubmed:volume
421
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
293-308
pubmed:dateRevised
2010-9-9
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Selective action of myasthenic syndrome antibodies on calcium channels in a rodent neuroblastoma x glioma cell line.
pubmed:affiliation
Department of Pharmacology, Royal Free Hospital Medical School, London.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't