| Loss of electrical excitability in an animal model of acute quadriplegic myopathy. | |
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MedLine Citation:
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PMID: 9485058 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In rats treated with high-dose corticosteroids, skeletal muscle that is denervated in vivo (steroid-denervated [S-D]) develops electrical inexcitability similar to that seen in patients with acute quadriplegic myopathy. In studies of affected muscles in vitro, the majority of S-D fibers failed to generate action potentials in response to intracellular stimulation although the average resting potential of these fibers was no different from that of control denervated muscle. The downregulation of membrane chloride conductance (G[Cl]) seen in normal muscle after denervation did not occur in S-D muscle. Although block of chloride channels in S-D muscle produced high specific membrane resistance, comparable to similarly treated control denervated muscle, and partially restored excitability in many fibers, action potential amplitude was still reduced in S-D fibers, suggesting a concomitant reduction in sodium current. 3H-saxitoxin binding measurements revealed a reduction in the density of the adult muscle sodium channel isoform in S-D muscle, suggesting that a decrease in the number of sodium channels present may play a role in the reduction of sodium current, although altered properties of channels may also contribute. The weakness seen in S-D muscle may involve the interaction of a number of factors that modify membrane excitability, including membrane depolarization, persistence of G(Cl), and reduced voltage-gated sodium currents. |
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Authors:
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M M Rich; M J Pinter; S D Kraner; R L Barchi |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Annals of neurology Volume: 43 ISSN: 0364-5134 ISO Abbreviation: Ann. Neurol. Publication Date: 1998 Feb |
Date Detail:
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Created Date: 1998-03-03 Completed Date: 1998-03-03 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 7707449 Medline TA: Ann Neurol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 171-9 Citation Subset: IM |
Affiliation:
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Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia 19104, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Action Potentials Animals Atrophy Chloride Channels / antagonists & inhibitors, metabolism Cholesterol / metabolism Denervation Disease Models, Animal Down-Regulation Female Male Membrane Potentials Muscle Contraction Muscle, Skeletal / innervation, metabolism, pathology Quadriplegia / physiopathology* Rats Rats, Sprague-Dawley Saxitoxin / pharmacology Sodium Channels / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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NS-01852/NS/NINDS NIH HHS; NS-08075/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Chloride Channels; 0/Sodium Channels; 35523-89-8/Saxitoxin; 57-88-5/Cholesterol |
| Comments/Corrections | |
Comment In:
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Ann Neurol. 1998 Feb;43(2):154-5
[PMID:
9485055
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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