Source:http://linkedlifedata.com/resource/pubmed/id/10212298
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
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| pubmed:dateCreated |
1999-5-7
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| pubmed:abstractText |
Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease that affects neurotransmitter release at peripheral synapses. LEMS antibodies inhibit Ca2+ currents in excitable cells, but it is not known whether there are additional effects on stimulus-secretion coupling. The effect of LEMS antibodies on Ca2+ currents and exocytosis was studied in bovine adrenal chromaffin cells using whole-cell voltage clamp in perforated-patch recordings. Purified LEMS IgGs from five patients inhibited N- and P/Q-type Ca2+ current components to different extents. The reduction in Ca2+ current resulted in smaller exocytotic responses to single depolarizing pulses, but the normal relationship between integrated Ca2+ entry and exocytosis (Enisch and Nowycky, 1996) was preserved. The hallmark of LEMS is a large potentiation of neuromuscular transmission after high-frequency stimulation. In chromaffin cells, stimulus trains can induce activity-dependent enhancement of the Ca2+-exocytosis relationship. Enhancement during trains occurs most frequently when pulses are brief and evoke very small amounts of Ca2+ entry (Engisch et al., 1997). LEMS antibody treatment increased the percentage of trains eliciting enhancement through two mechanisms: (1) by reducing Ca2+ entry and (2) through a Ca2+-independent effect on the process of enhancement. This leads to a paradoxical increase in the amount of exocytosis during stimulus trains, despite inhibition of Ca2+ currents.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/omega-Conotoxin GVIA
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| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
0270-6474
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
19
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3384-95
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:10212298-Adrenal Medulla,
pubmed-meshheading:10212298-Adult,
pubmed-meshheading:10212298-Aged,
pubmed-meshheading:10212298-Animals,
pubmed-meshheading:10212298-Autoantibodies,
pubmed-meshheading:10212298-Calcium Channels,
pubmed-meshheading:10212298-Cattle,
pubmed-meshheading:10212298-Cells, Cultured,
pubmed-meshheading:10212298-Chromaffin Cells,
pubmed-meshheading:10212298-Evoked Potentials,
pubmed-meshheading:10212298-Exocytosis,
pubmed-meshheading:10212298-Female,
pubmed-meshheading:10212298-Humans,
pubmed-meshheading:10212298-Immunoglobulin G,
pubmed-meshheading:10212298-Lambert-Eaton Myasthenic Syndrome,
pubmed-meshheading:10212298-Male,
pubmed-meshheading:10212298-Membrane Potentials,
pubmed-meshheading:10212298-Middle Aged,
pubmed-meshheading:10212298-Neuromuscular Junction,
pubmed-meshheading:10212298-Peptides,
pubmed-meshheading:10212298-omega-Conotoxin GVIA
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| pubmed:year |
1999
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| pubmed:articleTitle |
Lambert-Eaton antibodies inhibit Ca2+ currents but paradoxically increase exocytosis during stimulus trains in bovine adrenal chromaffin cells.
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| pubmed:affiliation |
Department of Neurobiology and Anatomy, Medical College of Pennsylvania and Hahnemann University, Philadelphia, Pennsylvania 19129, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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