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PubMed1995

Reduced lactate transport in denervated rat skeletal muscle.

The purpose of this study was to investigate the effect of the neural regulation of contractile activity on lactate transport in skeletal muscle. Contractile activity of the rat soleus muscle was abolished by denervating the hindlimb muscles in one leg (3 days) while the sham-operated contralateral hindlimb muscles served as a control. Three days after surgery, lactate transport into the soleus muscle was measured in vitro, using incubated soleus muscle strips. Lactate uptake by the denervated soleus muscle was reduced compared with control (P < 0.05). The diffusive component of lactate transport was unaltered by denervation (P > 0.05). These results translated into a reduction in lactate carrier-mediated transport capacity (-68%) in the denervated soleus (P < 0.05). These studies indicate that loss of contractile activity results in a decrement of lactate transport, which is probably due to a reduction in the number of lactate carriers in the sarcolemma. Our results suggest that the inherent activity of the muscle is important in maintaining the lactate transport system.

Animals↗
PubMed1994

The coexistence of embryonic and adult acetylcholine receptors in sarcolemma of mdx dystrophic mouse muscle: an effect of regeneration or muscular dystrophy?

In the sarcolemma of innervated dystrophic mdx mouse muscle we found the embryonic and the adult nicotinic acetylcholine receptor, where normally after innervation only the adult type would be expected, as can be shown with comparative data from patch-clamp experiments from wildtype and wildtype-denervated muscle. As a control to the dystrophic muscle we investigated wildtype bupivacaine-treated regenerating muscle and found both receptor types there, too. Therefore we conclude that the expression of the embryonic nicotinic acetylcholine receptor in the dystrophic muscle is not a characteristic of dystrophy but a consequence of muscle regeneration.

Animals↗
PubMed1987

Acetylcholine synthesis at the rat neuromuscular junction.

Acetylcholine (ACh) synthesis in homogenates of rat soleus muscles had two components. One component, specifically inhibited by bromoacetylcholine (BrACh), had a Km for choline of 0.26 mM; the other, resistant to BrACh, had a Km for choline of 45 mM. The component with a low Km was absent from denervated muscle, and was identical in kinetic terms to ACh synthesising activity in homogenates of sciatic nerve. It is therefore considered choline acetyltransferase (ChAT)-specific. The use of BrACh as a specific inhibitor of ChAT activity allowed the calculation of ACh synthesis at individual motor end-plates in the soleus muscle of the rat: 2.1 X 10(-3) nmol h-1. Since the number of muscle fibres and the number of motor units are known for this muscle, ACh synthesis per motor unit could be calculated: 0.15 nmol h-1. It is concluded that BrACh can be used as a specific inhibitor of ChAT activity in homogenates of skeletal muscle and that its use will obviate the necessity of dividing biopsied muscle or small rodent muscles into neural and aneural segments.

Acetylcholine↗
PubMed1984

Modification of synapses in androgen-sensitive muscle. I. Hormonal regulation of acetylcholine receptor number in the songbird syrinx.

The songbird syrinx is sexually dimorphic and responds to changes in blood testosterone levels with changes in muscle size and in activity of cholinergic enzymes (Luine, V., F. Nottebohm, C. Harding, and B.S. McEwen (1980) Brain Res. 192: 89-107). Here, we demonstrate that there is a sex difference in the number of acetylcholine receptors (AChRs) in the syrinx and that alterations in the levels of circulating testosterone can cause changes in AChR number in syringeal muscles. These results suggest that the size or number of endplates in the syringeal muscles may be increased by circulating testosterone. The time course of these effects was examined after increases in blood testosterone in females and decreases in males. We also examined the effect of increased testosterone in syrinx isolated from neural influences by denervation and found that denervated muscle responded to testosterone with an increase in acetylcholinesterase activity but not with increases in protein content or AChR number.

Acetylcholinesterase↗
PubMed1991

Denervation of the rabbit hind limb studied by 31-phosphorus magnetic resonance spectroscopy.

An animal model of muscle denervation was examined by 31P. magnetic resonance spectroscopy. The experiments demonstrated that there is a significant alteration in high and low energy phosphate metabolites in rabbit muscle after nerve section. The data show that there is an early change in the metabolites which appears to plateau at about six weeks. High resolution spectra of muscle cell extracts demonstrate qualitative alterations in the phosphate resonances found in the phosphodiester and phosphomonoester regions of the spectra. There would seem to be a time-related alteration in these components.

Adenosine Triphosphate↗
PubMed1999

Differential response of the membrane systems involved in excitation-contraction coupling to early and later postnatal denervation in rat skeletal muscle.

We compared the morphological features of the membrane systems involved in excitation-contraction (E-C) coupling during early postnatal development stages in rat skeletal muscles (tibialis anterior) denervated either at birth or 7 days after birth. Four obvious structural changes are observed in the arrangement of the transverse (T) tubule network and the disposition of triads following early postnatal denervation: (1) an increase in the longitudinal segments of the T tubule network, (2) changes in the direction and disposition of triads, (3) the appearance of caveolae clusters, (4) the appearance of pentads and heptads (i.e. a close apposition of two or three T tubule elements with three or four elements of terminal cisternae of sarcoplasmic reticulum). The increased presence of longitudinal T tubules parallels the loss of cross striations, and this in turn is due to misalignment of the myofibrils. The clusters of caveolae appear almost exclusively in muscle fibres denervated at birth, and pentads and heptads are more frequently observed in muscles denervated at 7 days. The differential growth of muscle fibres in response to denervation leads to the formation of abnormal membrane systems involved in the E-C coupling with very unique morphological features, which differ from the case of denervation in adult muscle fibres.

Age Factors↗
PubMed1997

Nitric oxide synthase and cyclic GMP-dependent protein kinase concentrated at the neuromuscular endplate.

Nitric oxide mediates diverse functions in development and physiology of vertebrate skeletal muscle. Neuronal type nitric oxide synthase-mu is enriched in fast-twitch fibers and binds to syntrophin, a component of the sarcolemmal dystrophin glycoprotein complex. Here, we show that cyclic GMP-dependent protein kinase type I, a primary effector for nitric oxide, occurs selectively at the neuromuscular junction, in mice and rats, and both neuronal type nitric oxide synthase-mu and cyclic GMP-dependent protein kinase type I remain at skeletal muscle endplates at least two weeks following muscle denervation. Expression of neuronal type nitric oxide synthase-mu and cyclic GMP-dependent protein kinase type I are up-regulated following fusion of cultured primary myotubes. Interestingly, the highest levels of neuronal type nitric oxide synthase-mu in muscle are found complexed with dystrophin at the sarcolemma of intrafusal fibers in muscle spindles. Localization of neuronal type nitric oxide synthase-mu and cyclic GMP-dependent protein kinase type I at the neuromuscular junction suggests functions for nitric oxide and cyclic GMP in the regulation of synaptic actions of intra- and extrafusal muscle fibers.

Animals↗
PubMed1982

Correlation of parvalbumin concentration with relaxation speed in mammalian muscles.

The physiological role of the Ca2+-binding protein parvalbumin in skeletal muscle has been investigated by measuring the parvalbumin content by HPLC in a variety of mammalian muscles, including man, and comparing the results with the respective muscle relaxation properties and fiber type compositions. The parvalbumin concentrations were highest in the skeletal muscles of the smallest animal investigated (mouse, gastrocnemius: 4.9 g/kg), which has the highest relaxation speed, and lowest in the larger animals (horse, deep gluteal muscle: less than or equal to 0.001 g/kg) and man (vastus, triceps: less than or equal to 0.001 g/kg), which have much lower relaxation speeds. Analysis of three type-homogeneous muscles of the guinea pig revealed highest parvalbumin concentrations (0.25 g/kg) in sartorius (type IIB) and lowest concentrations (less than or equal to 0.007 g/kg) in soleus (type I), consistent with the different half-relaxation times of fast and slow muscles. Denervation of the rat extensor digitorum longus, which increases the half-relaxation time from 9.4 to 19 msec, resulted in a 20% decrease of the parvalbumin content. Given this close correlation between parvalbumin content and relaxation speed in a variety of muscles and species, we suggest that parvalbumin is involved directly in the relaxation process in fast muscles.

Animals↗
PubMed2005

Acute systemic hypoxia elevates venous but not interstitial potassium of dog skeletal muscle.

Potassium release through ATP-sensitive potassium (K(ATP)) channels contributes to hypoxic vasodilation in the skeletal muscle vascular bed: It is uncertain whether K(ATP) channels on muscle cells contribute to the process. Potassium from muscle cells must cross the interstitial space to reach the vascular tissues, whereas that from vascular endothelium would have a higher concentration in venous blood than in interstitial fluid. We determined the effect of systemic hypoxia on arterial, venous, and interstitial potassium in the constant-flow-perfused gracilis muscles of anesthetized dogs. Hypoxia reduced arterial Po(2) from 138 to 25 and Pco(2) from 28 to 26 mmHg. Arterial pH and potassium were well correlated (r(2) = 0.9): Both increased in early hypoxia and decreased during the postcontrol. In denervated muscles, perfusion pressure decreased from 95 to 76 mmHg by the end of the hypoxic period; neither venous nor interstitial potassium was elevated. In innervated muscles, perfusion pressure increased from 110 to 172 mmHg by the 11th min of hypoxia and then decreased to 146 mmHg by the end of the hypoxic period; venous potassium increased from 5.0 to 5.3 mM, but interstitial potassium remained unchanged. Glibenclamide abolished both the increase in venous potassium and the hypoxic vasodilation in the innervated muscle. Thus skeletal muscle cells were unlikely to have contributed to the release of potassium, which was suggested to originate from vascular endothelium. The sympathetic nerve supply may play a direct or indirect role in the opening of K(ATP) channels under hypoxic conditions.

Acute Disease↗
PubMed1988

Induction of carbonic anhydrase III mRNA and protein by denervation of rat muscle.

Carbonic anhydrase III (CAIII) protein and mRNA amounts in fast- and slow-twitch rat muscles were examined after resection of the sciatic nerve. Striking changes occur in the fast-twitch anterior tibialis (AT) and extensor digitorum longus (EDL) muscles, where CAIII protein and mRNA are increased several-fold 16 days after denervation. The data suggest that these changes are regulated in part by changes in gene transcription and that they perhaps signal a fast-to-slow fibre type transition in these denervated muscles. AT and EDL show some differences in the effects of denervation, which are suggestive of variation in the timing of denervation-induced responses and/or the CAIII protein/mRNA turnover rates in the two muscles.

Actins↗
PubMed1985

Expression of cell adhesion molecule, N-CAM, in diseases of adult human skeletal muscle.

Antibody to the cell adhesion molecule N-CAM was used for analysis of cryostat sections using indirect immunofluorescence assay of human muscle biopsies from patients with a variety of muscle diseases. Positive staining was restricted to cases where haematoxylin and eosin staining revealed regenerating myofibers. N-CAM reactivity was specifically found associated with such regenerating fibres. No staining was found on normal adult, degenerating or necrotic fibres. In addition, in chronically denervated muscle disease there was no staining of either atrophic fibres or reinnervated fibres that tended to exist in fibre type specific groupings. N-CAM can therefore be regarded as a specific gene product of regenerating myofibres and is an additional marker of these fibres on biopsy of human muscle.

Adolescent↗
PubMed1991

Molecular alterations in the perijunctional region of frog skeletal muscle fibres following denervation.

The anatomical distribution of a frog skeletal muscle antigen was studied using immunofluorescence microscopy and a monoclonal antibody 3B6 that was produced against denervated skeletal muscle. In innervated muscles, the monoclonal antibody 3B6 stain was associated with the inner surface of the muscle plasma membrane at the endplate and myotendinous junction. After denervation, the monoclonal antibody 3B6 stain extended from the endplate laterally around the perimeter of muscle fibres and longitudinally well beyond the endplate for a total length of 600-1000 microns. The monoclonal antibody 3B6 stain thus forms a cylindrical structure centred on the endplate. This observation shows that denervation produces a non-homogeneous molecular change in skeletal muscle fibres: an antigen that is present in high concentrations at innervated endplates appears in restricted perijunctional regions of denervated muscle fibres. It further suggests that perijunctional regions of denervated muscle fibres differ from the remaining non-endplate regions in molecular composition and possibly also in function.

Animals↗
PubMed2000

Repression of myosin isoforms in developing and denervated skeletal muscle fibers originates near motor endplates.

During development of chicken pectoralis muscle, a neonatal myosin heavy-chain isoform is supplanted progressively by an adult isoform. This expression is under neuronal control. In this study we test the hypothesis that developmental myosin transformations are initiated near the motor endplate of each muscle fiber, thereafter progressing toward the fiber ends. By using immunocytochemical methods, pectoralis muscle from chickens aged 1-115 days after hatching were labeled by antibody against neonatal isoform. Ellipse minor axis and mean optical density of labeled and/or unlabeled fiber profiles from each bird were measured by computer image analysis. Acetylcholinesterase (AChE) activity was demonstrated histochemically. Using serial cross sections, we show that smaller fiber profiles are the tapered ends of larger fiber profiles. The largest fiber profiles (central regions of the fibers) were the first to lose their neonatal myosin during development. Motor endplates were localized by AChE activity to the central regions of the fibers. The pectoralis of mature chickens was denervated for 3, 7, 15, or 21 days. After 2 weeks' denervation, neonatal myosin is first reexpressed in the fiber ends. Dev Dyn 2000;217:50-61.

Animals↗
PubMed2006

Blood vessels and desmin control the positioning of nuclei in skeletal muscle fibers.

Skeletal muscle fibers contain hundreds to thousands of nuclei which lie immediately under the plasmalemma and are spaced out along the fiber, except for a small cluster of specialized nuclei at the neuromuscular junction. How the nuclei attain their positions along the fiber is not understood. Here we show that the nuclei are preferentially localized near blood vessels (BV), particularly in slow-twitch, oxidative fibers. Thus, in rat soleus muscle fibers, 81% of the nuclei appear next to BV. Lack of desmin markedly perturbs the distribution of nuclei along the fibers but does not prevent their close association with BV. Consistent with a role for desmin in the spacing of nuclei, we show that denervation affects the organization of desmin filaments as well as the distribution of nuclei. During chronic stimulation of denervated muscles, new BV form, along which muscle nuclei align themselves. We conclude that the positioning of nuclei along muscle fibers is plastic and that BV and desmin intermediate filaments each play a distinct role in the control of this positioning.

Animals↗
PubMed1999

Glycosaminoglycans treatment increases IGF-I muscle levels and counteracts motor neuron death: A novel nonanticoagulant action.

The present study shows that sciatic nerve crush in 2-day-old rats causes extensor digitorum longus (EDL) muscle atrophy and motor neuron loss and that treatment with glycosaminoglycans (GAGs) promotes muscle reinnervation, motor neuron survival, and markedly increases insulin-like growth factor-I (IGF-I) content in the denervated muscles. EDL muscle denervation-induced atrophy in saline-treated rats is progressive and reaches the greatest extent at 42 days after birth, which correlates with reduced EDL weight growth. There is also a partial reinnervation as shown by the number of reinnervated EDL muscle fibers (65.4% of control) and by the poor restoration of the indirect isometric twitch tension (62% of control) that is further reduced under tetanic stimulation (34% of control). The number of surviving motor neurons that innervate EDL muscle drops from 55 +/- 3 to 29 +/- 8. In GAGs-treated 42-day-old rats, the effects of neonatal nerve lesioning on EDL muscle atrophy and denervation are successfully reversed, and the isometric twitch tension and the capacity to hold tetanic stimulation are restored to almost control levels. The number of surviving EDL motor neurons is also increased to 43 +/- 4. Treatment with GAGs selectively affects IGF-I content in denervated hindlimb muscles, which is augmented from 7.02 +/- 0.71 ng/mg tissue to 25.72 +/- 0.7 in the EDL and from 3.2 +/- 0.18 to a robust 211 +/- 9.6 in the soleus.

Animals↗
PubMed1996

Innervation regulates myosin heavy chain isoform expression in developing skeletal muscle fibers.

The influence of innervation on primary and secondary myogenesis and its relation to fiber type diversity were investigated in two specific wing muscles of quail embryo, the posterior (PLD) and anterior latissimus dorsi (ALD). In the adult, these muscles are composed almost exclusively of pure populations of fast and slow fibers, respectively. When slow ALD and fast PLD muscles developed in ovo in an aneurogenic environment induced after neural tube ablation, the cardiac ventricular myosin heavy chain (MHC) isoform was not expressed. The adult slow MHC isoform, SM2, appeared by embryonic day 7 (ED 7) in normal innervated slow ALD but was not expressed in denervated muscle. Analysis of in vitro differentiation of myoblasts from fast PLD and slow ALD muscles isolated from ED 7 control and neuralectomized quail embryos showed no fundamental differences in the pattern of MHC isoform expression. Newly differentiated fibers accumulated cardiac ventricular, embryonic fast, slow SM1 and SM3 MHC isoforms. Nevertheless, the expression of slow SM2 isoform in myotubes formed from slow ALD myoblasts only occurred when myoblasts were cultured in the presence of embryonic spinal cord. Our studies demonstrate that the neural tube influences primary as well as secondary myotube differentiation in avian forelimb and facilitates the expression of different MHC, particularly slow SM2 MHC gene expression in slow myoblasts.

Acetylcholinesterase↗
PubMed1986

Effects of botulinum toxin induced muscle paralysis on endocytosis and lysosomal enzyme activities in mouse skeletal muscle.

The effects of botulinum toxin (type A) induced muscle paralysis on endocytosis and lysosomal enzyme activities in skeletal muscle were compared with the effects of surgical denervation. Muscle atrophy, measured as decrease in total muscle protein content, was as large or larger after botulinum toxin treatment as after denervation. Endocytic activity, measured as the in vitro uptake of horseradish peroxidase, and the specific activities of the lysosomal enzymes N-acetyl-beta-D-glucosaminidase and cathepsin D were all increased six days after denervation. Only the specific activity of cathepsin D was increased six days after botulinum toxin poisoning. The uptake of horseradish peroxidase and the specific activity of N-acetyl-beta-D-glucosaminidase were also increased eleven days after poisoning. Transverse sections of eleven days botulinum poisoned muscles from animals injected with horseradish peroxidase showed fibres with dense peroxidase staining similar to those seen in denervated muscle although they seemed to occur less frequently. The results show that increases in endocytic activity and lysosomal enzyme activities may occur in skeletal muscle without the presence of degenerating axons. The differences in effects of surgical denervation and botulinum toxin induced paralysis are discussed in terms of what is known about the mechanism of action of botulinum toxin and the possible functional roles of the two lysosomal enzymes studied.

Animals↗
PubMed2000

Effects of short- and long-term Schwann cell denervation on peripheral nerve regeneration, myelination, and size.

Poor functional recovery after peripheral nerve injury has been generally attributed to inability of denervated muscles to accept reinnervation and recover from denervation atrophy. However, deterioration of the Schwann cell environment may play a more vital role. This study was undertaken to evaluate the effects of chronic denervation on the capacity of Schwann cells in the distal nerve stump to support axonal regeneration and to remyelinate regenerated axons. We used a delayed cross-suture anastomosis technique in which the common peroneal (CP) nerve in the rat was denervated for 0-24 weeks before cross-suture of the freshly axotomized tibial (TIB) and chronically denervated CP nerve stumps. Motor neurons were backlabeled with either fluoro-ruby or fluorogold 12 months later, to identify and count TIB motor neurons that regenerated axons into chronically denervated CP nerve stumps. Number, size, and myelination of regenerated sensory and motor axons were determined using light and electron microscopy. We found that short-term denervation of < or =4 weeks did not affect axonal regeneration but more prolonged denervation profoundly reduced the numbers of backlabeled motor neurons and axons in the distal nerve stump. Yet, atrophic Schwann cells retained their capacity to remyelinate regenerated axons. In fact, the axons were larger and well myelinated by long-term chronically denervated Schwann cells. These findings demonstrate a progressive inability of chronically denervated Schwann cells to support axonal regeneration and yet a sustained capacity to remyelinate the axons which do regenerate. Thus, axonal interaction can effectively switch the nonmyelinating phenotype of atrophic Schwann cells back into the myelinating phenotype.

Animals↗