Linked Life Data

1119960

Source:http://linkedlifedata.com/resource/pubmed/id/1119960

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1975-5-29
pubmed:abstractText
The muscle membrane in myotonia congenita is characterized by a normal resting potential with a greatly increased resting resistance usually attributed to a decrease in membrane chloride permeability (PC1). In this report, the hypothesis that decreased PC1 alone can account for the repetitive action potentials of myotonia is tested with a mathematical model of the muscle membrane and is shown to be valid. Reduction of Pc1 to 20% of control values will produce myotonic activity in response to a single stimulus. Membrane resistance and potential approximate those found experimentally. The model predicts that increasing external K+ will aggravate myotonia due to a reduction of PC15 while decreasing Kout will prevent repetitive spiking. Further, myotonia can be prevented by reducing peak membrane sodium permeability or by shifting the voltage dependency of the membrane rate constants for sodium in a depolarizing direction. These results are shown to correlate well with clinical observtonia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0003-9942
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
175-80
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1975
pubmed:articleTitle
Myotonia. An evaluation of the chloride hypothesis.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.