Force and membrane potential in acetylcholine and potassium contractures of denervated mouse muscles

Abstract

Depolarization and contracture force (P) provoked by acetylcholine (ACh) and by K ions were studied in bundles dissected from mouse soleus muscles that had been denervated for 4-7 days. Cl-free solutions were used. The muscle fibres were depolarized by solutions containing 150 mM K or 10 microM ACh to nearly zero mV resulting in maximum P (Pmax). Threshold P was produced when the membrane was depolarized to more than about -60 mV by both agents. 50% Pmax was produced by [K] causing the membrane to depolarize to -42 mV, whereas a potential more positive than -20 mV was required for 50% Pmax to be produced when ACh was used. The rate of depolarization was always higher for ACh than for K. Pretreatment by 0.05 microM ACh (about threshold for P) did not affect the P-[K] relation appreciably showing that ACh did not "stabilize" the membrane. Nearly equal P was provoked by successive applications of just suprathreshold agent concentrations when the order of application was ACh----K but not with the reverse order. Hypertonicity (by addition of 300 mM sucrose to all solutions) caused PACh to decrease and PK to increase. It was concluded that the ACh receptors are located in the surface membrane of the muscle fibres, not in the T-system membranes.

Calcium current activation and charge movement in denervated mammalian skeletal muscle fibres.

“…A major characteristic of denervated muscles is the inability to sustain tension during prolonged contractions such as tetanus contraction and potassium contracture (Finol et al 1981;Dulhunty & Gage, 1985;Lorkovic, 1985;Obejero Pa,z, Delbono & Muchnik, 1986) although this is not the case in prolonged contracture such as that induced by caffeine (Gutmann & Sandow, 1965). Therefore a voltage-dependent mechanism may be involved in failure to sustain prolonged contraction.…”

Stable Gastric Pentadecapeptide BPC 157 and Striated, Smooth, and Heart Muscle

“…The concept was that BPC 157, given before or immediately after succinylcholine, counteracted succinylcholine effects [ 102 ]. Counteraction might include a local paralytic effect in the injected muscle or immediate leg contracture (also presented long after systemic muscle disability has abated) [ 102 ] (note, it was seen that chronically denervated muscles develop contracture and that the acetylcholine receptors develop over the entire surface of denervated skeletal muscle fibers after their motor nerve has been severed [ 149 ]). The initial agitations before muscle disability, the countless muscle twitches before complete muscle tonus loss, and the motionless laying were all counteracted [ 102 ].…”