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PubMed1977

The effects of experimental denervation and reinnervation on skeletal muscle fiber type and intramuscular innervation.

Porcine muscle has a unique grouped arrangement with 3-70 Type I fibers occurring in clusters surrounded by Type II fibers. The deep medial portion of the porcine semitendinosus exhibits a regular pattern of extensive Type I grouping whereas the superficial or lateral portion of the muscle exhibits Type II predominance. Mean values for terminal innervation ratios were 1.00 +/- 0.01 and 1.02 +/- 0.01 in normal superficial and deep semitendinosus respectively. Subterminal axons, therefore, do not branch intramuscularly and innervate only one muscle fiber in normal porcine muscle. Following nerve crush and subsequent reinnervation, fiber type conversion occurred which resulted in a fiber type grouping pattern dissimilar to the normal grouped arrangement. Significantly (P less than 0.01) elevated terminal innervation ratios (1.45-2.15) were measured in reinnervated muscle as a result of extensive branching of subterminal axons, but the percentage of Type I and Type II muscle fibers was unchanged. It was concluded that: (1) nerve crush causes distal nerve degeneration, loss of the normal fiber type pattern, and extensive collateral ramification of subterminal axons; (2) collateral reinnervation imposes a neuronal influence on muscle fibers which dictates transformation of all muscle fibers innervated by a single subterminal axon to a uniform histochemical profile; and (3) the type grouping observed in normal porcine muscle is not a result of neuronal influence mediated by collateral branching of subterminal axons.

Adenosine Triphosphatases↗
PubMed1987

Induction of rat muscle carbonic anhydrase by denervation demonstrated with immunofluorescence.

Immunofluorescence microscopy of carbonic anhydrase III (CA III) was performed on sections of rat anterior tibialis (AT), extensor digitorum longus (EDL) and soleus after denervation. In contralateral control muscles, CAIII was located only in type I fibres whereas following the operation, CAIII was markedly induced in type II fibers of all the muscles, most strikingly in EDL.

Animals↗
PubMed1991

Kinetic constants of the acetylcholine (ACh) receptor reaction deduced from the rise in open probability after steps in ACh concentration.

Outside-out patches of enzymatically dissociated adult and denervated mouse muscle fibers were superfused repetitively by pulses of acetylcholine (ACh) containing solution. Up to 300 channels opened simultaneously 300 microseconds after the beginning of a 1,000 microM ACh pulse corresponding to a peak current i of almost -1 nA. Single responses to ACh were averaged and the concentration dependence of i and of the rise time tr from 0.1 i to 0.9 i was measured. In adult receptors, i increased proportional to the second to third power of ACh concentration, whereas in embryonic-type receptors it was proportional to the first to the second power. tr increased from approximately 0.3 ms at 1,000 microM ACh to a plateau value of approximately 5 ms for adult and of approximately 10 ms for embryoniclike receptors at concentrations less than 10 microM ACh. The concentration dependence of i and tr was simulated using the standard model of ACh binding with different combinations of rate constants and two and three binding sites for ACh. The calculated curves were compared to the measurements and a set of well fitting rate constants was determined for adult and embryoniclike receptors. Three binding sites for ACh were necessary to fit the dose response for i for adult receptors. A method for deriving rate constants in a model of ACh-receptor interaction is described that avoids analysis of open-closed kinetics of single channels, which in rapid systems, as the ones studied here, are at the limit of the frequency response of the current measurement.

Acetylcholine↗
PubMed1997

Congenital hypomyelinating neuropathy: a reversible case.

A boy was born at 39 weeks gestation with severe weakness and hypotonia, fractured femurs, poor suck and swallow, and absent deep tendon reflexes. Electrodiagnostic studies revealed marked slowing of motor nerve conduction velocities and normal muscle electrical activity with no evidence of acute denervation. Muscle biopsy showed mild type 2 fiber predominance, and sural nerve biopsy revealed large axons without myelin, and axons with insufficient amount of myelin for their diameter. There was no evidence of inflammation or demyelination. Gradual clinical improvement in tone and strength occurred in a cephalocaudal direction. By 4 months, motor nerve conduction velocities and clinical examination were normal apart from absent deep tendon reflexes. On review at 19 months, motor development and neurological examination were completely normal. Pathogenesis of this reversible pathologically documented case of congenital hypomyelinating neuropathy is unclear. No evidence was found for an inflammatory, toxic, metabolic, or demyelinating cause. Abnormal expression of a developmental gene, as in reversible cytochrome oxidase deficiency, may be a cause of this neuropathy.

Axons↗
PubMed1998

Selective neurotomy of the tibial nerve in the spastic hemiplegic child: an explanation of the recurrence.

A series including 13 unilateral selective tibial neurotomies for spastic foot in hemiplegic children is reported. The results were considered excellent in three cases. Two cases needed additional corrective casts postoperatively. Eight cases had poor result with recurrence of the same deformity. The authors conclude that the effect of tibial neurotomy for spastic foot in hemiplegic children is transient in 61% of cases with a recurrence of the same deformity. Four of the patients with failed treatment underwent orthopedic surgery with muscle biopsies. Histologic data clearly demonstrate that previously denervated muscle fibers were reinnervated carrying into extensive motor units. This finding can explain the recurrence of the foot spasticity and deformity in neurotomized children.

Adolescent↗
PubMed1978

Amantadine: neuromuscular blockade by suppression of ionic conductance of the acetylcholine receptor.

Amantadine hydrochloride decreases the sensitivity of denervated mammalian muscle to iontophoretically applied acetylcholine. The drug depresses the amplitude of the end-plate current and reverses the slope of the relation between half-decay time and membrane potential suggesting that it alters the ionic conductance that is mediated by the acetylcholine receptor. Binding studies confirm that amantadine acts on the ion conductance modulator rather than the acetylcholine receptor.

Acetylcholine↗