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At least 1,189 records · Page 66Linked to original sources
PubMed1998

Rimmed vacuoles with beta-amyloid and ubiquitinated filamentous deposits in the muscles of patients with long-standing denervation (postpoliomyelitis muscular atrophy): similarities with inclusion body myositis.

In the chronically denervated muscles of patients with prior paralytic poliomyelitis, there are secondary myopathic features, including endomysial inflammation and rare vacuolated fibers. To assess the frequency and characteristics of the vacuoles and their similarities with those seen in inclusion body myositis (IBM), we examined 58 muscle biopsy specimens from patients with prior paralytic poliomyelitis for (1) the presence of rimmed vacuoles; (2) acid-phosphatase reactivity; (3) Congo-red-positive amyloid deposits; (4) electron microscopy, searching for tubulofilaments; and (5) immunoelectron microscopy, using antibodies against beta-amyloid and ubiquitin. We found vacuolated muscle fibers in 18 of 58 (31%) biopsies, with a mean frequency of 2.06 +/- 0.42 fibers per specimen. The vacuoles contained acid phosphatase-positive material in 6 of the 18 (33.30%) specimens and stained positive for Congo red in five (27.80%). By immunoelectron microscopy, the vacuoles contained 5.17 +/- 0.13 nm fibrils and 14.9 +/- 0.31 nm filaments that immunoreacted with antibodies to beta-amyloid and ubiquitin in a pattern identical to the one seen in IBM. We conclude that vacuolated muscle fibers containing filamentous inclusions positive for amyloid and ubiquitin are not unique to IBM and the other vacuolar myopathies but can also occur in a chronic neurogenic condition, such as postpoliomyelitis. The chronicity of the underlying disease, rather than the cause, may lead to vacuolar formation, amyloid deposition, and accumulation of ubiquitinated filaments.

Amyloid beta-Peptides↗
PubMed1980

Ultrastructural localization of acid phosphatase in denervated and diabetic striated muscles.

Catabolism in denervated and diabetic rat skeletal muscle undergoing accelerated protein degradation has been investigated with methods for demonstrating acid phosphatase ultrastructurally. Control muscles displayed strong acid phosphatase activity in lateral sacs and in sparse secondary hysosomes distributed mainly near nuclear poles. Muscles from diabetic rats and, to a lesser extent, 2-day denervated rats, revealed increased secondary lysosomes apparently derived from fusion of mitochondria with acid-phosphatase-reactive vesicles and cisternae. The latter were interpreted as possibly originating from T tubules. Reaction product was also noted in the junctional folds of the motor end plate of a denervated muscle. At the longer post denervation intervals studied, deposits indicative of acid phosphatase were dispersed throughout the sarcoplasm with greater concentration in the I band and appeared more abundant in denervated than in contralateral control muscles. The enzymatic basis for the sarcoplasmic deposits and other deposits was confirmed by their absence from cytochemical controls, which included incubation in substrate-free medium, heat or NaF inactivation of enzyme, and exposure sequentially to PbNO3 and NaH2PO or PbNO3 and beta-glycerophosphate.

Acid Phosphatase↗
PubMed1992

Leakage of carbonic anhydrase III from normal and denervated rat skeletal muscle following contractile activity.

Skeletal muscle extracellular carbonic anhydrase III was investigated in anesthetized rats by a microdialysis technique. A small dialysis probe was inserted into the tibialis anterior (TA) muscle and perfused continuously. Perfusates were collected before and during muscle contraction, induced by electrical stimulation of the muscle or of the sciatic nerve. In the perfusate of resting normal and denervated muscle, the concentration of CA III was 10 to 12 ng/mL, as measured by a radioimmunosorbent technique. During contractile activity, the concentrations of CA III increased markedly in the normal and denervated muscle. A TA muscle suspended in physiological saline behaved similarly, even though the leakage before and during contraction was higher than in vivo. The results show that skeletal muscle leaks CA III both in vivo and in vitro, a leakage which was markedly increased by contractile activity. The microdialysis technique should also be useful in humans to study the efflux of various proteins from different kinds of diseased or fatigued muscles.

Animals↗
PubMed1996

[Metabolic changes in denervated skeletal muscles].

Section of the motor nerve of skeletal muscles produces severe atrophy and causes dramatic changes in biochemical properties of the muscles. Progressive decrease of oxidative and glycolytic activity, increased protein and purine degradation are prominent features of muscular atrophy. Denervation leads also to rapidly developing insulin resistance in skeletal muscles.

Animals↗
PubMed1995

Secretion of plasminogen activator and lysosomal enzymes from mouse skeletal muscle: effect of denervation.

Levels of hydrolytic enzymes increase in skeletal muscle after denervation and their activities in the extracellular matrix appear to be important for interaction between muscle and nerve. Using enzymatic assays for beta-glucuronidase, beta-galactosidase, and plasminogen activator, we show that secretion of these enzymes from mouse skeletal muscle increases after denervation and that drugs interfering with the secretory pathway or the reuptake of enzymes modulate this release. Thus, brefeldin A inhibited secretion of plasminogen activator activity and mannan increased secreted amounts of beta-glucuronidase, but not of beta-galactosidase, in denervated muscle. In innervated muscle, brefeldin A decreased secreted activity of plasminogen activator, but mannan had no effect on secretion of either beta-glucuronidase or beta-galactosidase. Furthermore, secretion of plasminogen activator was temperature dependent. These observations, together with previous studies, suggest that secretion of hydrolytic enzymes from adult skeletal muscle may be of physiological significance in nerve-muscle communication.

Animals↗
PubMed1993

Denervated chicken breast muscle displays discoordinate regulation and differential patterns of expression of alpha f and beta tropomyosin genes.

The expression of the alpha fast (alpha f) and beta tropomyosin (TM) genes has been analysed with muscle-specific and common cDNA probes after unilateral nerve section of the pectoralis major muscle (PM) in 4-week-old chickens. The following were observed in denervated muscles. (1) The beta TM mRNA, which was repressed during development, reaccumulates in a biphasic curve with the increase in the beta TM protein lagging behind the changes in its mRNA. Accordingly, no beta TM is seen in products translated in vitro from total and polyA+ RNA obtained 1 week after denervation. No such translation block is seen with RNA obtained from control or muscles denervated for 6 weeks. (2) No changes in the alpha fTM mRNA and corresponding protein are observed. (3) RNA processing of the two genes is not changed. (4) In the contralateral muscles, transitory increases in alpha f and beta TM mRNAs are observed while the corresponding proteins remain unchanged. Our data suggest that muscle fibres display early and long-term responses to the loss of neural input which might result from a combination of changes produced by regenerative processes and reprogramming of existing fibres. Moreover, in contrast to normal development, no reciprocal changes of alpha f and beta TM expression are seen in denervated muscles.

Animals↗
PubMed1993

Mechanical response of lizard skeletal muscles to disuse: II. Effect of short-term denervation.

The gastrocnemius muscles of Uromastix hardwickii were used to determine the effects of the absence of neural influence on them. For this purpose, the muscles were denervated for 7 days and were used to record isometric twitch and tetanus. The contraction parameters thus obtained from the denervated muscles were then compared with their own controls. The isometric tensions and time dependent tension parameters were significantly lower in the denervated muscles. The time dependent parameters, peak duration in twitch and duration of active state in twitch were however, found to be unaffected by short-term denervation with the exception of twitch/tetanus half relaxation time ratio, which was significantly higher in the denervated muscles. The denervation effects observed on the mechanical contraction behaviour of the gastrocnemius muscle have been discussed in terms of electrical excitation, excitation-contraction coupling and cross bridge interaction.

Animals↗
PubMed1993

Degradation of two AChR populations at rat neuromuscular junctions: regulation in vivo by electrical stimulation.

The effect of electrical stimulation on the stability of junctional ACh receptors (AChR) on soleus muscles of Wistar rats was compared to that of denervation and reinnervation. Denervation causes the degradation rate of the slowly degrading AChRs (Rs) at the neuromuscular junction to accelerate and be replaced by rapidly degrading AChRs (Rr), while reinnervation restabilizes the accelerated Rs. Electrical stimulation initiated at the time of denervation prevented the acceleration of the Rs. It could not, however, reverse the effect of denervation if initiated after the AChRs became destabilized, nor could it slow the degradation rate of the Rr. We conclude that electrical stimulation of denervated muscle downregulates the expression of the Rr and prevents the destabilization of Rs.

Animals↗
PubMed1999

BEN/SC1/DM-GRASP expression during neuromuscular development: a cell adhesion molecule regulated by innervation.

BEN/SC1/DM-GRASP is a cell adhesion molecule belonging to the Ig superfamily that is transiently expressed during avian embryogenesis in a variety of cell types, including the motoneurons of the spinal cord. We have investigated the pattern of BEN expression during neuromuscular development of the chick. We show that both motoneurons and their target myoblasts express BEN during early embryonic development and that the protein becomes restricted at neuromuscular contacts as soon as postsynaptic acetylcholine receptor clusters are observed in muscle fibers. Muscle cells grown in vitro express and maintain BEN expression even when they fuse and give rise to mature myotubes. When embryos are deprived of innervation by neural tube ablation, BEN expression is observed in muscle fibers, whereas, in control, the protein is already restricted at neuromuscular synaptic sites. These results demonstrate that all myogenic cells intrinsically express BEN and maintain the protein in the absence of innervation. Conversely, when neurons are added to myogenic cultures, BEN is rapidly downregulated in muscle cells, demonstrating that innervation controls the restricted pattern of BEN expression seen in innervated muscles. After nerve section in postnatal muscles, BEN protein becomes again widely spread over muscle fibers. When denervated muscles are allowed to be reinnervated, the protein is reexpressed in regenerating motor axons, and reinnervation of synaptic sites leads to the concentration of BEN at neuromuscular junctions. Our results suggest that BEN cell adhesion molecule acts both in the formation of neuromuscular contacts during development and in the events leading to muscle reinnervation.

Activated-Leukocyte Cell Adhesion Molecule↗
PubMed1982

Post-tetanic potentiation and inhibition in single fibres isolated from frog semitendinosus muscle.

The twitch contractions of single fibres from the frog semitendinosus, innervated and denervated, were studied after a brief period (2-3 sec) of conditioning stimulation (CS), at frequencies varying from 1-120/sec. Twitch potentiation was consistently observed in denervated fibres at all rates of CS used. Maximal potentiation was attained within the first 12 sec after the end of CS, which then decayed progressively. The overall duration of the effect, in general, was longer than 5 min. The time course of potentiated twitches was slightly shortened. Inhibition preceding potentiation was the prevailing effect on innervated fibres under the present conditions. Inhibition appeared either after a short interval (500 msec of less) between the end of CS and the beginning of the subsequent twitch, or after several repetitions of the conditioning schedule. The latter form of inhibition was replaced by potentiation when the corresponding fibres were allowed to rest for 60 min before further conditioning stimulations. Maximal inhibition was attained shortly after the end of CS, which then progressively disappeared. On occasion inhibition lasted longer than 5 min. The time course of inhibited twitches was slightly enlarged. After fatigue, CS produced twitch inhibition on innervated fibres. In denervated muscles the effect was either potentiation or inhibition. These results are discussed according to the data in the literature.

Action Potentials↗
PubMed1997

Lysosomal proteolysis in distally or proximally denervated rat soleus muscle.

We examined the mechanism of accelerated proteolysis in denervated rat soleus muscles. The soleus was denervated by severing either the tibial nerve (proximal, short stump) or sciatic nerve (distal, long stump) at 24, 48, 72, or 96 h before excision. Twenty-four hours after denervation, the extent of atrophy was similar for proximal and distal denervation, although lysosomal latency declined in both groups. After 48 and 72 h, denervation resulted in a decline in protein content, an increase in in vitro protein degradation, and a decline in lysosomal latency, all of which were greater in proximally denervated than in contralateral distally denervated muscles. These differences between acute responses of proximally and distally denervated muscles suggest the retention of some factor in the longer nerve stump that attenuates atrophy. After 96 h, total protein loss, protein degradation, and lysosomal latency were similar for proximal and distal denervation, suggesting the loss of axoplasmic flow from the long nerve stump.

Animals↗
PubMed1998

Nerve-dependent factors regulating transcript levels of glycogen phosphorylase in skeletal muscle.

1. Muscle glycogen phosphorylase (MGP), the rate-limiting enzyme for glycogen metabolism in skeletal muscle, is neurally regulated. Steady-state transcript levels of the skeletal muscle isozyme of MGP decrease significantly following muscle denervation and after prolonged muscle inactivity with an intact motor nerve. These data suggest that muscle activity has an important influence on MGP gene expression. The evidence to this point, however, does not preclude the possibility that MGP is also regulated by motor neuron-derived trophic factors. This study attempts to distinguish between regulation provided by nerve-evoked muscle contractile activity and that provided by the delivery of neurotrophic factors. 2. Steady-state MGP transcript levels were determined in rat tibialis anterior (TA) muscles following controlled interventions aimed at separating the contributions of contractile activity from axonally transported trophic factors. The innervated TA was rendered inactive by daily epineural injections of tetrodotoxin (TTX) into the sciatic nerve. Sustained inhibition of axonal transport was accomplished by applying one of three different concentrations of the antimicrotubule agent, vinblastine (VIN), to the proximal sciatic nerve for 1 hr. The axonal transport of acetylcholinesterase (AChE) was assessed 7, 14, and 28 days after the single application of VIN. 3. MGP transcript levels normalized to total RNA were reduced by 67% in rat TA, 7 days after nerve section. Daily injection of 2 microg TTX into the sciatic nerve for 7 days eliminated muscle contractile activity and reduced MGP transcript levels by 60%. 4. A single, 1-hr application of 0.10% (w/v) VIN to the sciatic nerve reduced axonal transport but did not alter MGP transcript levels in the associated TA, 7 days after treatment. Application of 0.10% VIN to the sciatic nerve also did not affect IA sensory or motor nerve conduction velocities or TA contractile function. 5. Treatment of the sciatic nerve with 0.40% (w/v) VIN for 1 hr reduced axonal transport and decreased MGP transcript levels by 50% within 7 days, but also reduced sensory and motor nerve conduction velocities and depressed TA contractile function. 6. Myogenin, a member of a family of regulatory factors shown to influence the transcription of many muscle genes, including MGP, was used as a molecular marker for muscle inactivity. Myogenin transcript levels were increased following denervation and after treatment with TTX or 0.40% VIN but not after treatment with 0.10% VIN. 7. The results suggest that MGP transcript levels in TA are regulated predominantly by muscle activity, rather than by the delivery of neurotrophic factors. Intrinsic myogenic factors, however, also play a role in MGP expression, since denervation did not reduce MGP transcript levels below 30% of control TA. The dominant influence of activity in the regulation of MGP contrasts with the proposed regulation of oxidative enzyme expression, which appears to depend on both activity and trophic factor influences.

Animals↗