Nonequivalence of surgical and natural denervation in dystrophic mouse muscles

Law, Peter K.; Atwood, Harold L.

doi:10.1016/0014-4886(72)90167-7

Cited by 42 publications

(2 citation statements)

References 20 publications

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“…of the ReJ-129 strain (Jackson Labs, Bar Harbor, ME). The muscles were secured in an experimental chamber filled with circulating oxygenated (gassed with 95% 0 2 , 5% Con) Krebs-Ringer solution at 37°C (pH 7.4) of the following composition: 1 18.4 mM NaC1, 4.7 mM KCI, 2.52 mM CaC12, 25.01 mM NaHCO:+, 11 mM glucose, 1.18 mM MgS04, 1.18 mM K3P04.…”

Section: Materlals and Methodsmentioning

confidence: 99%

Membrane alterations in skeletal muscle fibers of dystrophic mice

Kerr

Sperelakis

1983

Muscle and Nerve

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Skeletal muscle fibers from dystrophic mice and littermate controls (ReJ-129) were characterized electrically and then injected with an intracellular marker. In this way they could be identified for examination with an electron microscope to correlate the relative time course of electrical and ultrastructural alterations resulting from the dystrophic process. On the average, dystrophic muscle fibers displayed decreased membrane potentials (-59 +/- 1.2 vs -79 +/- 0.7 mV for normals), decreased specific membrane resistivity (517 +/- 27 vs 642 +/- 34 omega-cm2 for normals), and depressed action potential (AP) maximum rates of rise (+Vmax) (352 +/- 9 vs 417 +/- 9 V/s for normals) and amplitudes (92 +/- 1.2 vs 102 +/- 1.0 mV for normals) at an experimentally polarized membrane potential of -90 mV. Membrane resistivity and AP +Vmax were decreased even in those fibers from dystrophic muscles that displayed normal ultrastructure (classified visually and by ratio of sarcoplasmic reticulum to total cell volume). These findings support the membrane hypothesis of muscular dystrophy that membrane lesions are the primary lesion in the disease process.

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Section: Materlals and Methodsmentioning

confidence: 99%

Membrane alterations in skeletal muscle fibers of dystrophic mice

Kerr

Sperelakis

1983

Muscle and Nerve

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“…In other respects, the diaphragm seems to be atypical in its involvement in this disease. Thus, the resting membrane potential, the time constant and the input resistance of the dystrophic fibres did not differ significantly from normal; the hind limb muscles usually demonstrate a reduced resting membrane potential (Harris, 1971) and changes in both time constant and input resistance (McComas & Mossawy, 1966;Law & Atwood, 1972).…”

Section: Resultsmentioning

confidence: 99%

PHARMACOLOGICAL ASPECTS OF NEUROMUSCULAR TRANSMISSION IN THE ISOLATED DIAPHRAGM OF THE DYSTROPHIC (Rej 129) MOUSE

Harris

Ribchester

1979

British J Pharmacology

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Some aspects of the pharmacology of neuromuscular transmission have been studied in the isolated diaphragm of the normal and dystrophic mouse. The effects of (+)‐tubocurarine and atropine on the indirectly elicited twitch responses of the dystrophic diaphragm were indistinguishable from normal. Intracellular recording techniques revealed no significant differences between the rise time, time to half decay, frequency and amplitude of miniature endplate potentials (m.e.p.ps) recorded in dystrophic muscle fibres, compared to those recorded in normal muscle fibres. Transmitter null potential, the size of the available store of transmitter, the probability of release of the transmitter, and the characteristics of endplate potentials (e.p.ps) of dystrophic muscle fibres did not differ from normal. The quantum contents of e.p.ps generated in response to nerve stimulation of 0.1 to 100 Hz were consistently larger in dystrophic muscle fibres than in normal muscle fibres, but the differences were not statistically significant under the conditions of the experiment.

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Reduced axonal transport of 10S acetylcholinesterase in dystrophic mice

Brimijoin

Schreiber

1982

Muscle and Nerve

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Extracts of extensor digitorum longus muscle, atria, brain, and sciatic nerve from phenotypically normal and dystrophic ReJ/129 mice were subjected to sucrose density gradient ultracentrifugation, and the amounts of acetylcholinesterase (AChE) activity associated with each major enzyme form were determined. Normal muscle showed approximately equivalent amounts of the 4S, 10S, and 16S forms of AChE, while dystrophic muscle was relatively deficient in 10S AChE and relatively oversupplied with 4S AChE. This abnormality was not present in the other tissues examined. However, as measured by the 24-hour accumulation of enzyme activity proximal to a ligature on the sciatic nerve, the axonal transport of 10S AChE was only about one third as great in dystrophic as in normal nerve. This result is consistent with the view that the reduction in the amount of this enzyme form in dystrophic muscle could be related to disturbances in a transport-dependent trophic interaction between nerve and muscle.

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Nonequivalence of surgical and natural denervation in dystrophic mouse muscles

Cited by 42 publications

References 20 publications

Membrane alterations in skeletal muscle fibers of dystrophic mice

Membrane alterations in skeletal muscle fibers of dystrophic mice

PHARMACOLOGICAL ASPECTS OF NEUROMUSCULAR TRANSMISSION IN THE ISOLATED DIAPHRAGM OF THE DYSTROPHIC (Rej 129) MOUSE

Reduced axonal transport of 10S acetylcholinesterase in dystrophic mice

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