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PubMed1977

The effect of denervation on subsequent in vitro induction of myotonia.

In order to study the influence of innervation on myotonia, an attempt was made to induce myotonia in previously denervated rat hemidiaphragm preparations in vitro with use of 2,4-dichlorophenoxy acetic acid (2,4-D) and low chloride solutions. Prior denervation prevented the onset of myotonia in both media except during the first 24 hours after nerve section. On the basis of already available data, we propose that the reduced potassium conductance accompanying denervation may be the main factor preventing induciton of myotonia in denervated muscle.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1988

Immunostaining of motor nerve terminals by IgM M protein with activity against gangliosides GM1 and GD1b from a patient with motor neuron disease.

We demonstrated the binding of an IgM monoclonal protein, obtained from a patient with motor neuron disease, with known antibody activity against gangliosides GM1, GD1b, and asialo GM1, to neuromuscular junctions in guinea pig gastrocnemius muscle, using an indirect immunofluorescence technique. Staining disappeared after delipidation of muscle sections. Denervated muscle sections showed no labeling at the neuromuscular junction after incubation with the patient's serum. This indicates presynaptic binding of the IgM M protein and supports the concept that IgM monoclonal antibody to nerve terminal determinants may underlie a motor neuron disorder.

Animals↗
PubMed1991

Fibrillation potentials do not originate in type 1 muscle fibers?

Electrophysiological and muscle histochemical studies of denervated muscle were performed simultaneously in order to determine the relationship between fibrillation potentials and muscle fiber type. Fibrillation potentials recorded in the soleus muscle 2 weeks after resection of the sciatic nerve revealed a lower firing rate than in the extensor digitorum longus (EDL) muscle of the same rats. The majority of muscle fibers stained for adenosine triphosphatase (ATPase) activity after preincubation at pH 9.4, 4.6, and 4.3 in the soleus muscle were type 1 fibers, while most of those in the EDL were of type 2. Moreover, one of the rats, which demonstrated no fibrillation potentials in the soleus muscle, was found to have no type 2A or 2B fibers histochemically, in the same soleus muscle. These findings suggest that fibrillation potentials may not originate in type 1 fibers.

Action Potentials↗
PubMed1974

The binding of tetrodotoxin and alpha-bungarotoxin to normal and denervated mammalian muscle.

1. The binding of [(3)H]tetrodotoxin and [(125)I]iodo-alpha-bungarotoxin to innervated and denervated rat diaphragm muscle has been measured.2. A saturable component of tetrodotoxin binding, which was inhibited by saxitoxin, was detected in addition to considerable non-saturable binding. The saturable component had an equilibrium constant of K = 6.1 nM (limits 4.7-7.8 nM) and binding capacity M = 2.5 f-mole/mg wet wt. (limits 2.1-2.8 f-mole/mg).3. If the saturable component consisted of one-to-one binding of tetrodotoxin to sodium channels, the density of sodium channels would be about 21/mum(2) of surface membrane, a figure similar to that found in other excitable membranes.4. After denervation the specific tetrodotoxin binding, as measured by the ratio M/K, fell by a factor of 2.8. This change appeared to be due to a fall in binding capacity rather than a decrease in affinity.5. After denervation the maximum rate of rise of the action potential fell by 27% and became partially resistant to tetrodotoxin. The maximum rate of rise was at first reduced by tetrodotoxin in similar concentrations to those affecting normal muscle, but even large concentrations which completely blocked normal muscle only reduced the maximum rate of rise by a factor of about 2.6. Detubulation with glycerol did not appreciably affect the tetrodotoxin sensitivity of normal or denervated muscle.7. Tetrodotoxin resistance was not observed after denervation of the frog sartorius muscle.8. [(125)I]iodo-alpha-bungarotoxin binding amounted to 3.8 +/- 0.7 f-mole/mg in innervated muscle and 44.5 +/- 2.1 f-mole/mg in denervated muscle. Most of the uptake was inhibitable by (+)-tubocurarine.9. The increase in the labelled bungarotoxin binding is much larger than the specific tetrodotoxin binding of innervated muscle, which renders implausible the possibility that the acetylcholine receptors which appear after denervation are related to the tetrodotoxin resistant-sodium channels.

Action Potentials↗
PubMed1988

Effect of soluble factors from nerve and muscle on alpha-bungarotoxin binding sites in isolated sarcolemmal membranes of the rat.

1. Sarcolemmal membranes were isolated from normal and from denervated muscles and the specific binding of [125I]-alpha-bungarotoxin to the membranes was determined. 2. Cytosol prepared from either slow (soleus) or fast (extensor digitorum longus) muscle increased the toxin binding. Similar effects were seen with cytosol from muscles which had been denervated 5 to 7 days previously and with cytosol from sciatic nerve. A purified preparation of a bacterial phospholipase C also produced this effect. 3. Bathing medium in which normal or denervated muscles had been incubated, increased the toxin binding to normal membranes, but the normal bathing medium decreased the binding to membranes prepared from denervated muscles. 4. The possibility that pre-existing latent acetylcholine receptors can be activated by intracellular factors released from muscles is discussed.

Animals↗
PubMed1976

Cholinergic sites in skeletal muscle. I. Denervation effects.

Cholinergic interactions in systems derived from rat skeletal mixed muscle are detailed. The isotherms of the binding of [125I]diiodo-alpha-bungarotoxin over the range of 10(-10)-10(-5) M toxin have been separated into a "nonspecific" component exclusive to the toxin and a "specific" component that binds both the toxin and d-tubocurarine. The "specific" component appears to reflect two independent sets of binding sites. One of the sets has an affinity constant on the order of 10(9) M-1. Following denervation, the number of sites in this high-affinity set begins to increase after 3 days, reaches a peak (28-fold higher than normal) on the 8th day, and begins to decline. Similar results are obtained when sensitivity of this set to an antibody derived from patients with myasthenia gravis is examined. This sensitivity is reflected by the inhibition of the alpha-bungarotoxin binding by the myasthenic IgG fraction. Following denervation, sensitivity first appears on day 3 progresses coincidentally with the increase in new sites in the set. The charcteristics of this set suggest that it represents the acetylcholine receptor and that the new sites appearing during the course of denervation are extrajunctional receptor sites. The interaction with the myasthenic IgG indicates an antigenic difference between junctional and extrajunctional receptors. The second set of specific binding sites has an affinity constant on the order of 10(5) M-1. The number of sites in this set increases only fivefold as a result of denervation. The increase also begins between days 2 and 3. The definition of this low affinity set of sites is not presently clear.

Animals↗
PubMedDate not supplied

[Spectroscopic study of myosin from denervated rabbit muscles].

Spectra of tryptophan UV-fluorescence and UV-absorption of myosin isolated 30 days after denervation of white skeletal muscles of rabbit were studied. It has been observed that fluorescence intensity of such myosin in the maximum decreases. This decrease becomes more pronounced after purification of protein from admixtures. It has been shown that after denervation the absorption at 260 nm increases, however, the difference disappears after myosin purification. The data obtained point to a change of myosin structural state after denervation.

Animals↗
PubMed1988

Changes in denervated skeletal muscle of amiodarone-fed mice.

Prolonged dosing of mice with amiodarone produced a myopathy characterized by autophagic vacuolation and phospholipid inclusions. A previous morphological study had shown that amiodarone did not affect the rate of nerve regeneration after sciatic nerve crush. In the present study, reinnervation was assessed by the reappearance of miniature endplate potentials that confirmed that axonal regeneration and motor reinnervation was not affected by amiodarone. However, there was a marked delay in the recovery of motor function in the amiodarone-treated mice. Denervation was found to induce an extensive necrosis of muscle fibers in the deeper parts of fast-twitch muscles. Histochemical studies showed that type 1 fibers were spared, necrosis affecting mainly type 2 fibers with relatively high oxidative enzyme activity (fast-twitch oxidative fibers). Biochemical studies showed a significant increase in the amount of amiodarone and its metabolite in denervated muscle of amiodarone-treated mice when compared with contralateral, normally innervated muscles.

Amiodarone↗
PubMed1992

Changes in mast-cell distribution in skeletal muscle after denervation.

Motor nerves are known to govern the structure of skeletal muscle. In the normal guinea pig diaphragmatic muscle, we found that mast cells were predominantly located in the central tendon. Following denervation, these cells became more numerous in the muscle itself than in the tendon. Therefore, nervous trophic influences are exerted on other tissue elements besides those which sustain transmission and contraction. Ascertaining mast-cell distribution in biopsies may help to elucidate denervation effects in motor neuron disease.

Animals↗
PubMed1978

Muscular dystrophy contrasted with denervation: different mechanisms underlying spontaneous fibrillations.

The data reviewed in this paper indicate that spontaneous fibrillations do not involve a cholinergic mechanism since non-depolarizing anticholinesterase drugs such as Mestinon fail to increase spontaneous fibrillations in denervated muscle. Fibrillation potentials are related to the changes in electrical properties of the membrane of denervated muscle fibres which lead to the appearance of spontaneous subthreshold depolarizations, sometimes triggering a propagated potential. Fibrillations seem to appear in cycles and this may depend on the depression of spontaneous depolarization by muscle activity itself. Fibrillations are also an important feature of Duchenne muscular dystrophy and polymyositis, but they have not been found in Landouzy-Dejerine muscular dystrophy. These "myopathic" fibrillations probably arise from subthreshold depolarizations in the membrane of muscle fibre segments which have been functionally or anatomically isolated from the end-plate by a pathological lesion (Fig. 4). Experimental demonstration of spontaneous fibrillations in baboon biceps muscles after extrajunctional myotomies indicates that such an isolated muscle fibre segment can indeed develop and sustain spontaneous fibrillation activities. Studies of motor unit potentials in myopathies by "coherent" electromyography disclose linked potentials after the main potential in Duchenne dystrophy, but not in Landouzy-Dejerine muscular dystrophy. The linked potentials are signs of collateral innervation by sprouts of the motor axons. The fact that linked potentials occur in Duchenne dystrophy, including in obviously dystrophic motor units (Fig. 5), shows that such motor axons are quite healthy and able to sprout efficiently. The muscle fibres thus innervated collaterally are probably the ones which fibrillated and were deprived of trophic motor control as a result of myopathic lesions of the type considered in Fig.4. This correlation receives support from the finding that both spontaneous fibrillations and linked potentials are lacking in Landouzy-Dejerine muscular dystrophy, which obviously presents a different type of muscle lesion.

Acetylcholine↗
PubMed1993

The effects of chronic administration of chloroquine and quinacrine on the response of normal and denervated smooth muscle to agonist drugs.

The functional effects of chronic administration of 60 mg kg-1 chloroquine or quinacrine given as daily intraperitoneal injections for 84 days on normal and denervated expansor secundariorum muscles, a smooth muscle from the wing of chicks wholly innervated by noradrenergic nerves, have been investigated. Administration of quinacrine, but not chloroquine, blocked responses to noradrenergic nerve stimulation. Surgical denervation abolished responses to nerve stimulation. Contraction of the expansor muscle induced by noradrenaline was not changed by chronic administration of chloroquine or quinacrine, and both drugs did not influence denervation supersensitivity of expansor muscles to noradrenaline. Expansor muscles were unresponsive to acetylcholine (ACh) and histamine, but muscles from chicks chronically treated with chloroquine and quinacrine were responsive to ACh and histamine. Denervation also restored the response of expansor muscles to ACh and histamine and the responses were greater for denervated muscles from chronically treated chicks; these changes were more marked with quinacrine. Expansor muscles were contracted by potassium chloride (KCl) and 5-hydroxytryptamine (5-HT), and chronic treatment increased the responsiveness of expansor muscles to KCl. Denervation increased the responsiveness of expansor muscles to KCl and 5-HT; this effect was more pronounced in denervated muscles from quinacrine-treated chicks. The findings indicate that chronic administration of quinacrine sensitizes smooth muscles to agonist drugs by blocking noradrenergic transmission to induce postjunctional changes and exerting a direct action on the smooth muscle; these actions are less pronounced with chloroquine administration.

Acetylcholine↗