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Slow calcium current is not reduced in malignant hyperthermic porcine myotubes
Author(s) -
Gallant Esther M.,
Balog Edward M.,
Beam Kurt G.
Publication year - 1996
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199604)19:4<450::aid-mus4>3.0.co;2-b
Subject(s) - malignant hyperthermia , myogenesis , endocrinology , ryanodine receptor , medicine , dihydropyridine , chemistry , calcium , skeletal muscle , patch clamp , endoplasmic reticulum , antagonist , calcium channel , voltage dependent calcium channel , membrane potential , electrophysiology , biology , biochemistry , receptor , anesthesia
Malignant hyperthermia‐susceptible (MHS) pigs express a sarcoplasmic reticulum (SR) Ca 2+ ‐release channel mutation that results in lower than normal contractile thresholds in skeletal muscles. In adult MHS pig muscles the L‐type calcium current (I s ) is also reduced. We tested the hypothesis that there is a causal relationship between I s and the lower contractile threshold by recording I s from MHs and normal porcine myotubes using the whole cell patch‐clamp technique. Current voltage relationships for both MHS and normal myotubes were similar, with peak I s between +20 and +30 mV. Maximum I s amplitudes were not different (normal: 4976 ± 566 pA; MHS: 6516 ± 1088 pA) nor was I s specific density (normal: 9.0 ± 0.8; MHS: 8.8 ± 1.1 pA/pF). In both MHS and normal myotubes, both the dihydropyridine antagonist PN200 –110 (200 nmol/L) and holding the membrane potential at −10 mV for 5 min decreased I s significantly (by more than 50%). There was no apparent direct relationship between the mutation in the SR Ca 2+ ‐release channel and lowered I s . We concluded that reduced I s in adult MHS pig muscles may be a secondary effect of the SR Ca 2+ ‐release channel mutation on muscle development. © 1996 John Wiley & Sons, Inc.