Altered e-c coupling in triads isolated from malignant hyperthermia -susceptible porcine muscle. El-Hayek, Roque, Masafumi Yano, Bozena Antoniu, James R. Mickelson, Charles F. Louis, and Noriaki Ikemoto. Department of Muscle Research, Boston Biomedical Research Institute, Boston, MA 02114; Departments of Veterinary Biology and Biochemistry, University of Minnesota, St Paul, MN 55108; and Department of Neurology,
APStracts 2:0048C, 1995.
Triad vesicles were isolated from normal (N) and homozygous malignant hyperthermia susceptible (MHS) porcine skeletal muscle, and two types of SR Ca2+ release were investigated: 1) polylysine-induced Ca2+ release (direct stimulation of the junctional foot protein) and (2) depolarization-induced Ca2+ release (stimulation of the junctional foot protein via the dihydropyridine receptor). At submaximal concentrations of polylysine examined, the rates of induced Ca2+ release from the MHS triads were greater than from normal triads. The T-tubules of polarized triads were depolarized by the K+aeNa+ ionic replacement protocol. Higher grades of T-tubule depolarization resulted in higher rates of Ca2+ release from both MHS and normal triads, but when compared at a given grade of T-tubule depolarization, the release rate was always greater from the MHS than from normal triads. Thus, the activity of the SR Ca2+ release channel is always higher in MHS than in normal muscle at a given sub-maximal dose of release trigger. This difference is observed when the channel is stimulated directly by polylysine, or indirectly via a depolarization-induced activation of the T-tubule dihydropyridine receptor. 

Received 28 June 1994; accepted in final form 7 December 1994
APS Manuscript Number C0366-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1994 The American Physiological Society.
Published in APStracts on 27 February 1995.