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PubMed1982

Importance of pathway formation for nodal sprout production in partly denervated muscles.

Experiments were carried out to investigate possible factors controlling nodal sprout growth in partly denervated mouse gluteal muscles. Pretreatment of the muscle with botulinum toxin for up to 20 days, which produces denervation-like change and elicits terminal and nodal sprouting, increased reinnervation by terminal sprouting after partial denervation but did not alter the rate of reinnervation by nodal sprouts. This implies that nodal sprout growth is not limited by the development of an adequate growth stimulus from denervated muscle. A disto-proximal gradient of degeneration was observed in denervated intramuscular nerves in the electron microscope, suggesting that nodal sprout growth may be modulated by the availability of endoneurial pathways sufficiently degenerated to permit reinnervation by nodal sprouts, although the initial outgrowths from nodes of Ranvier may appear in response to a growth stimulus from denervated muscle.

Animals↗
PubMed1998

Changes of sonographic, magnetic resonance tomographic, electromyographic, and histopathologic findings within a 2-month period of examinations after experimental muscle denervation.

This study compares sonographical, histopathological, magnetic resonance imaging (MRI), and electromyographical (EMG) findings following acute muscle denervation. We performed an experimental denervation of the supraspinatus and infraspinatus muscles on 35 New Zealand white rabbits by segment resection of the suprascapular nerve. The sonographical appearance of the supraspinatus muscle was followed and documented at short time intervals within a 2-month follow-up period. The sonographical, histopathological, and MRI changes due to denervation suggest a regular pattern. Apart from the reduction of the muscle diameter, there were considerable sonographical signs of denervation with an increase of echointensity and inhomogenicity of echotexture that appeared on day 14 after injury, and progressed continuously with time. MRI revealed a remarkable increase in signal intensity 3 weeks after denervation and reproducible T2 times. Pathological spontaneous activity on EMG could also be detected from day 14 after injury. Conventional histopathological staining methods (H&E, NADH, ATPase, basic and acid phosphatase) confirmed denervation and absence of reinnervation. The first nonspecific histopathological changes were seen 11 days after denervation in the form of moderately atrophic fibers. Typical histopathological signs of denervation appeared 3 weeks after nerve dissection. In summary, EMG, ultrasound, MRI, and histopathology each showed first abnormalities after about 2 weeks. In addition to EMG, sonography and MRI can document the course of muscle atrophy and mesenchymal abnormalities in neurogenic muscle lesions.

Animals↗
PubMed1989

Conditioning lesion effects on rat sciatic nerve regeneration are influenced by electrical stimulation delivered to denervated muscles.

The rate of regeneration and the initial delay of the fastest growing fibers of the rat sciatic nerve were electrophysiologically evaluated after a freeze at mid-thigh. A prior section or a prior freeze at the ankle level increased the rate of regeneration and decreased the initial delay with different magnitudes. These phenomena are named 'conditioning lesion effects'. A daily electrical stimulation transcutaneously delivered to the foot sole muscles from the day following their denervation by the prior lesion did not modify the increased rate of regeneration but prevented the decrease of the initial delay whatever the type of the prior lesion. Therefore, the initiation of earlier sprouting of the parent axons seems to be specifically controlled by a signal associated with muscle denervation properties.

Animals↗
PubMed1981

Effects of extracts of denervated muscles on the morphology of cultured muscle cells.

Previously, trophic effects of extracts from whole chick embryos and from innervated muscles on cultured muscle cells were described. The present study demonstrated similar effects of extracts from 10-days denervated chick muscles. Extracts from innervated as well as from denervated muscles exsanguinated in vivo with saline prior to dissection showed only marginal trophic activity, suggesting a major contribution of serum components to the trophic effects of tissue extracts. Indeed, serum of adult chicks appeared to have a trophic action similar to that of chick embryo extract.

Animals↗
PubMed1984

Muscle fiber type differentiation and satellite cell populations in normally grown and neonatally denervated muscles in the rat.

To examine the neural influence upon fiber type differentiation in developing muscles, newborn rats were subjected to sciatic nerve dissection, and the denervated extensor digitorum longus (EDL) (white) and soleus (red) muscles were examined in chronologic sequence by means of histochemistry and electron microscopy. The skeletal muscles in the newborn rats were undifferentiated (type 2C fibers seen on ATPase staining) and contained numerous myotubes. In the controls, the type 2C fibers started to differentiate at around 5 days and had almost completed type differentiation by 30 days in EDL and by 90 days in soleus muscles. On the other hand, none of the fibers in the neonatally denervated muscles developed into well differentiated type 1 and 2 A fibers, but both the EDL and soleus showed long-lasting type 2C and 2B populations. The satellite cells in the denervated EDL and soleus muscles decreased in number at the same rate as in the control muscles with maturation. The absence of a neural supply in the developing muscles induced a delay in muscle fiber type differentiation but did not influence the satellite cell populations in either EDL or soleus muscles.

Animals↗
PubMed1992

Muscle denervation in peripheral arterial disease.

Muscle function is often severely impaired in peripheral arterial disease (PAD), but the effects of repeated ischemic events upon nerve and muscle are incompletely characterized. We performed comprehensive electrophysiologic studies and skeletal muscle histologic analysis in six patients with unilateral PAD and five control subjects matched for age and activity level. In the PAD patients, all ischemic legs showed both electrophysiologic and histologic evidence of chronic partial denervation-reinnervation restricted to distal muscles. Two of the PAD patients had evidence of milder distal denervation in the nonischemic legs. Two of the controls had denervation in at least one leg, but in each case electrophysiologic findings were pathognomonic of L-5 and S-1 radiculopathies. All other control legs and nonischemic legs were normal. These results suggest that recurrent ischemia associated with PAD may cause muscle denervation, which may be one of the mechanisms responsible for decreased exercise performance in these patients.

Action Potentials↗
PubMed2000

Magnetic resonance imaging of denervated muscle: comparison to electromyography.

The purpose of the study is to further assess the usefulness of short TI (time to inversion) recovery (STIR) magnetic resonance imaging (MRI) in detecting denervation of skeletal muscle compared to needle electromyography (EMG). Ninety subjects with clinical evidence of peripheral nerve injury or radiculopathy underwent STIR MRI and EMG of the affected limb. In 74 (82%) of these subjects, a positive correlation was found between STIR MRI and EMG (P < 0.009). STIR MRI has a relative sensitivity of 84% and specificity of 100% for detecting denervation. A subset of 28 subjects underwent quantitative assessments of signal intensity ratio (SIR) from the STIR MRI. The rank order correlation coefficient between the SIR and abnormal spontaneous activity on EMG was 0.70 (P < 0.001). Increased signal intensity on STIR MRI corresponds closely with spontaneous activity on EMG in denervated muscle. Although less sensitive than EMG in detecting muscle denervation, STIR MRI may be a useful adjunctive diagnostic tool in this setting.

Adult↗
PubMed1977

The role of extracellular calcium in the contractions produced by acetylcholine in chronically denervated muscle.

1 Acetylcholine-induced contractions of the isolated chronically denervated soleus muscle of the mouse consist of two phases, but both phases are equivalent to the contracture phase seen in vivo.2 Low [Ca(2+)](0) (0.5-1.5 mM) augmented peak tension, as well as the rate of relaxation, of the first phase, but inhibited the second phase. Ethyleneglycol-bis-(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) or La(3+) (2 mM) also inhibited the second phase, but not the first.3 It was concluded that the first phase requires Ca(2+) release from the sarcoplasmic reticulum, and is terminated by inactivation of the contractile process. The second phase is caused by the entry of activator Ca(2+) from the extracellular space.4 Increasing [Ca(2+)](o) to 5 or 10 mM after the addition of acetylcholine caused a contraction, starting after a delay of about 50 seconds. EGTA or La(3+) added during the second phase of the acetylcholine contraction caused relaxation after a much shorter lag time.5 It is concluded that most of the Ca(2+) entering from the extracellular fluid is taken up by the sarcoplasmic reticulum.6 The acetylcholine second phase was augmented in low (25 mM) [Na(+)](0). It is concluded that Na(+) and Ca(2+) compete for the acetylcholine controlled ionic channels.7 Isolated chronically denervated diaphragm muscles were less sensitive to acetylcholine and the contraction usually consisted of a first phase only.8 It is concluded that sequestration of Ca(2+) entering from the extracellular fluid is more complete in the diaphragm.

Acetylcholine↗
PubMed2006

[Inhibitor of nitric oxide synthase on the denervated muscle atrophy].

OBJECTIVE: To study the effect of the competitive inhibitor of nitric oxide synthase N(G)-nitro-L-arginine methyl ester (L-NAME) on the denervated muscle atrophy. METHODS: A model of the denervated gastrocnemius at the right lower limb was established in 36 SD adult rats. The rats were randomly divided into two groups: the L-NAME group (Group A) and the control group (Group B). L-NAME 10 mg/kg daily was injected into the denervated gastrocnemius in Group A, and normal saline was injected into the denervated gastrocnemius in Group B. At 2, 4 and 8 weeks after operation, the rate of the muscle wet weight preservation, the cross section area of the myocyte, the protein amount, and the percentage of the apoptotic muscle cells were measured respectively and the ultramicrostructure of the myocyte was observed. RESULTS: At 2 and 4 weeks after operation, the rate of the muscle wet weight preservation, the cross section area of the myocyte, and the protein amount were significantly greater in Group A than in Group B; however, the percentage of the apoptotic muscle cells was significantly smaller in Group A than in Group B. The observation of the ultramicrostructure of the myocyte showed that an injection of L-NAME could protect the ultramicrostructure of the myocyte. At 8 weeks after operation, there was no significant difference between the two groups in the above-mentioned parameters. CONCLUSION: The nitric oxide synthase inhibition can delay the denervated muscle atrophy.

Animals↗
PubMed1984

Lysosomal and energy enzyme activities in hypertrophied rat soleus muscle after denervation.

Muscle hypertrophy was induced in the soleus muscle of young rats by tenotomy of the gastrocnemius and plantaris muscles. Three and 7 days afterwards the sciatic nerve was sectioned. The loss of weight of muscles subjected to this combined procedure three days after denervation was 30-40%. Lysosomal enzyme activities (acid phosphatase, alpha-glucosidase, beta-galactosidase and N-acetyl-beta-D-glucosaminidase) and energy enzyme activities (lactate dehydrogenase, LDH, triose-3-phosphate dehydrogenase, TPDH , D-hexokinase, HK and citrate synthase, CS) were determined 3 days after denervation, 3, 7 and 10 days after hypertrophy had been induced and 3 days after denervation of hypertrophying muscles on day 3 and 7. Normal non-operated rats of corresponding body weight served as controls and their enzyme activities were estimated on the same day. In the course of muscle hypertrophy, the 4 lysosomal enzyme activities increased progressively. Although 3 days' denervation of control muscles did not alter lysosomal enzyme activities, denervation of hypertrophying muscles greatly enhanced the activity of these enzymes. Enzymes of energy metabolism were affected to a lesser degree. The results suggest that denervation of hypertrophying muscles causes more extreme changes in muscle weight and lysosomal enzyme activities than denervation alone. The possible implications of this finding are discussed in relation to the rapid atrophy.

Animals↗
PubMed1979

Dynamic properties of partially denervated muscle.

The mechanical and electrical properties of the partially denervated first dorsal interosseous muscle were measured in 14 patients and 14 normal control subjects. The following variables were studied during isometric contraction: maximum voluntary contraction; maximum rate of rise of tension in a rapid voluntary contraction; amplitude, rate of rise, time to peak, and duration of peak of the compound muscle action potential; twitch force, maximum rate of rise, contraction time, and half-relaxation time; and tetanic (50 Hz) force, rate of rise, and tetanus/twitch ratio. The force produced during repetitive stimulation of the ulnar nerve at 10, 20, 50, and 100 impulses per second was also analyzed. The major findings were: (1) decreased load bearing (voluntary contraction, twitch, and tetanus), (2) prolonged twitch contraction times and half-relaxation times, (3) decreased tetanus/twitch ratio, and (4) preserved rate of rise of tension.

Adult↗
PubMed1986

Phospholipids, prostaglandin E2, and proteolysis in denervated muscle.

Soleus muscles of rats were studied up to 16 days after sciatic nerve transection. At the end of this period the denervated soleus muscles exhibited decreased content of diphosphatidylglycerol (-44%), normal level of phosphatidylethanolamine, and increased contents of phosphatidylcholine (+24%), sphingomyelin (+48%), lysophosphatidylcholine (+110%), phosphatidylinositol (+37%), and phosphatidylserine (+40%) per milligram of tissue protein. In studies in vitro, prostaglandin E2 (PGE2) release and tyrosine release by denervated soleus muscles were 319 and 141%, respectively, greater than those of sham muscles. An almost complete inhibition of PGE2 release with 5 X 10(-4) M aspirin or 2.8 X 10(-6) M indomethacin had no effect on tyrosine release of sham muscles or the stimulated tyrosine release of the denervated muscles. Addition of 5 X 10(-5) M cycloheximide in the medium resulted in 63% inhibition of PGE2 release by both groups of muscles; concomitant absolute increments in tyrosine releases by denervated and sham muscles did not statistically differ. In the presence of both 5 X 10(-5) M cycloheximide and 5 X 10(-4) M aspirin in the medium, PGE2 production by denervated and sham muscles was inhibited 87% while tyrosine release of denervated muscles was 108% higher than that of sham animals. It is concluded that 1) atrophy of denervated soleus muscle is associated with stimulated activity of tissue phospholipase A2, increased production of prostaglandin E2, increased total proteolytic rate, and unchanged rate of protein synthesis; 2) acute inhibition of PGE2 production does not inhibit the stimulated proteolysis in denervated muscle; and 3) cycloheximide inhibits PGE2 production by muscle.

Animals↗
PubMed2006

The denervated muscle: facts and hypotheses. A historical review.

Denervation changes in skeletal muscle (atrophy; alterations of myofibrillar expression, muscle membrane electrical properties, ACh sensitivity and excitation-contraction coupling process; fibrillation), and their possible causes are reviewed. All changes can be counteracted by muscle electrostimulation, while denervation-like effects can be caused by the complete conduction block in muscle nerve. These results do not support the hypothesis that the lack of neurotrophic, non-motor factors plays a role in denervation phenomena. Instead they support the view that the lack of neuromotor discharge is the only cause of the phenomena and that neuromotor activity is an essential factor in regulating muscle properties. However, some experimental results cannot apparently be explained by the lack of neuromotor impulses, and may still suggest that neurotrophic influences exist. A hypothesis is that neurotrophic factors, too feeble to maintain a role in completely differentiated, adult muscles, can concur with neuromotor activity in the differentiation of immature, developing muscles.

Animals↗
PubMed2001

Preservation of denervated muscle form and function by clenbuterol in a rat model of peripheral nerve injury.

The effects of clenbuterol in preserving the form and function of muscle after unilateral sciatic nerve division and epineural repair were investigated in a rat model. The drug (a beta2-adrenoceptor agonist) was administered daily for six weeks by gastric gavage (10 microg/kg body weight), interrupted every 5 days by a 2 day omission of dosing to avoid drug desensitization. Clenbuterol reduced the loss of wet weight, total protein, muscle fibre cross sectional area and (in part) contractile forces in denervated hindlimb muscles, with most effects lasting until reinnervation. The effects were dependent on muscle type, with slow-twitch oxidative muscle (soleus) and mixed-fibre (gastrocnemius) showing greater sensitivity to the drug than fast-twitch muscle (extensor digitorum longus). Anabolic effects on the contralateral innervated muscles tended to be small. The results suggest a potential for the adjuvant use of selective beta -adrenoceptor agonists in the management of peripheral nerve injuries in humans.

Adrenergic beta-Agonists↗
PubMed1994

The use of preoperative muscle denervation and postoperative electrostimulation to maximize functional results in microneurovascular muscle transplantation.

A study of the morphologic and physiologic adaptations of orthotopic microneurovascular gracilis musculocutaneous transplantations was done on dogs, using postoperative electrostimulation or prior denervation, compared to controls. Postoperative electrostimulation helped preserve enzyme activity at muscle synapses. Prior denervation demonstrated the enhancement of nerve-fiber penetration into the transplanted muscle, producing better restoration of transplant contraction than in controls. These techniques maximize the functional results of dynamic gracilis musculocutaneous microneurovascular transplantation in the dog model.

Animals↗
PubMed2002

Skeletal muscle denervation increases satellite cell susceptibility to apoptosis.

Peripheral motor nerve trauma severely compromises skeletal muscle contractile function. Satellite cells respond to denervation by dividing multiple times, ultimately fusing with other satellite cells or myocytes to form new muscle fibers. After chronic denervation, satellite cell numbers decline dramatically, impairing the ability to regenerate and repair myofibers. This satellite cell depletion may contribute to the mechanical deficit observed in denervated or reinnervated muscle. Apoptosis, an evolutionarily conserved form of cell suicide, is a potential mechanism for satellite cell depletion in denervated skeletal muscle. This work tested the hypothesis that skeletal muscle denervation increases satellite cell susceptibility to apoptotic cell death. Adult rats underwent sciatic nerve transection to denervate the distal hindlimb musculature; rats of similar age without the operation served as controls. Two, 6, 10, or 20 weeks after denervation (n = 6 each group), the gastrocnemius and soleus were excised, enzymatically digested, and plated for satellite cell culture. After reaching 95 percent confluence, satellite cells were treated for 24 hours with tumor necrosis factor-alpha (20 ng/ml) and actinomycin D (250 ng/ml), known pro-apoptotic agents. Immunostaining for activated caspases, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and hematoxylin and eosin staining were performed to identify apoptotic satellite cells. Percentages of apoptotic cells were quantified histomorphometrically. In addition, the presence or absence of bcl-2 and bax was determined by Western blot analysis of control, 6 weeks of denervation, and 10 weeks of denervation specimens. At 6 and 10 weeks after nerve transection, TUNEL and caspase activity were increased more than two-fold in satellite cells isolated from denervated muscle compared with those isolated from control muscle (p < 0.05). In all experimental groups, retention of adherence to the collagen-coated substrate was strongly associated with satellite cell survival. Western blot analysis revealed that adherent satellite cells from all groups expressed both bcl-2 and bax. These data support the authors' hypothesis that skeletal muscle denervation increases satellite cell susceptibility to apoptotic cell death. Apoptosis may play a causative role in the depletion of satellite cells in long-term denervated skeletal muscle.

Animals↗
PubMed2005

Characterization of matrix metalloproteinases in denervated muscle.

In a nerve crush model of denervation, we examined muscle matrix metalloproteinase (MMP) expression, localization and activity. In normal muscle, MMP mRNA levels were low, and immunohistochemically MMPs were distributed around the muscle fibre with MMPs-3, -7 and -9 also staining at the neuromuscular junction. Seven days after nerve crush, muscle MMP immunoreactivity, especially MMP-12 and MMP-14, became irregularly distributed. At 20 days reinnervation of the muscle was observed, and some restitution of the normal pattern of immunoreactivity was noted concomitant with a higher level of MMP mRNA expression. In situ zymography showed that MMP activity was very weak in normal muscle whereas it was increased up to 40 days following denervation. Our results suggest that MMPs in muscle are involved in the tissue changes following denervation. Further experiments are required to test the hypothesis that MMP inhibition may be beneficial in protecting muscle from excessive remodelling following denervation and therefore improve reinnervation.

Animals↗