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PubMed1993

[The increase in endocytosis of mouse skeletal muscle after denervation and the proliferation of satellite cells].

The relationship between increase of endocytosis and proliferation of satellite cells in mouse skeletal muscle was studied by biochemical and culture methods in vitro. The results indicated that: (1) 4 d or 6 d after denervation, increase of endocytosis and proliferation of satellite cells in denervated muscle were induced. (2) Actinomycin D inhibited activation of satellite cells and endocytosis in normal muscle. (3) While in denervated muscle, actinomycin D inhibited proliferation of satellite cells as well as increase of endocytosis, but could not prevent muscle atrophy after denervation. These results imply that proliferation of satellite cells and increase of endocytosis in the muscle may concur to the appearance of some factors after denervation, or increase in endocytosis is a mere result of proliferation of satellite cells.

Animals↗
PubMed1977

Potassium and chloride conductances in normal and denervated rat muscles.

The membrane conductance of rat muscles (mainly gastrocnemius (G) and soleus (S)) was measured by using the two-microelectrode technique and the current point clamp method. Thin muscle bundles were washed in Tris chloride and Tris propionate solutions containing 6 mM K. The current strength was always 5 x 10-9 A and the steady-state membrane voltage was about 5 mV. The average chloride conductance (gcl, in mumho/cm2) of normal muscles was 845 (G) and 1,025 (S). The potassium conductance (gk) was 99 (G) and 161 (s). In separate measurements, the contribution of the chloride conductance (gcl) to the total membrane conductance (gm) was 89% for normal G and S. Two weeks after denervation the average gcl decreased to 440 in G and 191 in S; gk increased to 205 in G and to 364 in S in the presence of 0.1 mM Ca in solution; the increase in gk was less when measurements were made in the presence of 3mM Ca and 1 mM Mg. The contribution of gcl to gm was 60% in G and 30% in S in 14-day denervated muscles. The coefficient of variation for gcl/gk in 30 normal and 46 denervated muscles was 0.91 and 0.46, respectively. The curve representing the voltage-current relationship of muscles washed in Cl-free solutions containing 60 mM K was S-shaped in normal and in denervated muscles, but the changes in slope were less marked in the latter.

Animals↗
PubMed1986

Effect of denervation on primate laryngeal muscles: a morphologic and morphometric study.

Primate intrinsic laryngeal muscles studied consisted of Type I and Type II fibres. Type II fibres were larger than Type I fibres. The coefficient of variance of these muscles suggested that the fibre-size variation was similar in all of these muscles. Denervation resulted in shrinking of Type II fibres at two weeks in all the muscles, while at four weeks the thyroarytenoid showed an inflammatory reaction and far greater reduction in size than the other muscles. At eight weeks, however, all the muscles were fibrosed. We conclude that laryngeal muscles begin to show evidence of denervation at two weeks and are fibrosed in eight weeks. The thyroarytenoid muscle showed inflammatory degeneration, while the posterior cricoarytenoid and cricothyroid muscles showed classical changes of denervation. These findings should have clinical significance in the timing of reinnervation procedures.

Animals↗
PubMed1998

[Experimental study on denervated skeletal muscle autotransplantation in the rhesus monkey].

OBJECTIVE: This study was to provide a scientific basis for clinical application of denervated muscle transplantation. METHODS: A rhesus monkey was used in this experiment. The denervated extensor digitorum brevis (EDB) and the extensor hallucis brevis (EHB) of the rhesus monkey were autotransplanted in the sacrospinal muscle, and they were biopsied at intervals and stained with HE, Bielshowsky and enzyme. The specimen were examined with light and electro-microscope. RESULTS: The metabolism of the denervated muscle was lower than the normal. There was muscle regeneration and growing nerve fibers in the graft 12 weeks after transplantation. CONCLUSION: Denervated muscle can regenerate in oxygen-deficient environment. If the denervated muscle is in contact with normal muscle, the nerve of the recipient muscle will grow into the graft.

Animals↗
PubMed1986

Decreased acetylcholine receptor content in denervated skeletal muscles infused with nerve extract.

The influence of a concentrated extract of soluble substances from the sciatic nerve upon the acetylcholine receptor (AChR) content in the soleus muscle of adult rats was examined by in vivo infusions. Internal and membrane-inserted AChR were quantitated by the specific binding of 125I-alpha-bungarotoxin (a-BuTX). Interestingly, the nerve extract had no apparent effect unless the soleus muscle was also denervated at the start of the infusion. Then, after 66 hr, substantially less (60-80%) binding of 125I-a-BuTX to AChR was observed compared to denervated solei that did not receive an infusion of nerve extract. However, the concentration of protein in the nerve extract had to exceed 5 mg/ml before this effect was evident. Infusions of phosphate-buffered saline, bovine serum albumin, rat liver extract, or human transferrin had no striking effect upon AChR. The prevention of the characteristic denervation-induced increase in non-junctional AChR by an active component in the nerve extract may be due to a trophic signal for decreased synthesis of AChR, but it is also possible that the degradation of AChR was increased.

Animals↗
PubMed1994

Effects of denervation on posterior cricoarytenoid muscle physiology and histochemistry.

The effects of chronic posterior cricoarytenoid muscle denervation were assessed at 3 and 7 months in 26 animals following resection of 10 cm of recurrent laryngeal nerve with stump ligation. The physiology of denervation was characterized by a decrease in contraction strength and an increase in contraction time. The reduction in contraction strength reflected the loss in muscle weight and atrophic changes in fiber density and diameter. A change in muscle composition occurred because of the increased susceptibility of fast-twitch (type 2) fibers to degeneration. However, the compositional change alone could not account for the slowing of muscle contraction. Muscle fibrosis was negligible at 3 months, but encompassed one third of the fiber population by 7 months. In view of the irreversible nature of fibrosis, this study suggested that clinical intervention to rescue denervated posterior cricoarytenoid muscle fibers should be delayed no longer than 7 months to improve the chances for full recovery.

Animals↗
PubMed1991

Dystrophin-related protein in the fetal and denervated skeletal muscles of normal and mdx mice.

The amino acid sequence of the polyclonal antibodies we developed against the carboxyl terminus of the dystrophin-related protein, the putative gene product of B3 cDNA, had no homologous sequence to the dystrophin molecule except for two amino acids located at its ends for immunization. By immunohistochemical examination in C57B1/10ScSn and C57B1/10ScSn-mdx mice we found that the DRP was expressed on the surface membrane of fetal muscle fibers, was assembled at the neuromuscular junctions of the mature muscle fibers, and reappeared on the surface membrane of muscle fibers after denervation. Its localization was similar to that of the acetylcholine receptor, suggesting that DRP is one of the cytoskeletons which organize and stabilize the cytoplasmic domain of the acetylcholine receptor.

Aging↗
PubMed1991

Hemodynamic effects of nicotine in canine skeletal muscle.

Studies were conducted in 36 artificially ventilated, anesthetized dogs to clarify hemodynamic effects of nicotine in resting gracilis muscle. In Series 1, effects of intravenous nicotine (36 micrograms/kg/min) were evaluated in (i) intact muscles (Condition 1), (ii) denervated muscles (Condition 2), (iii) denervated muscles following local alpha-adrenergic blockade (Condition 3), (iv) denervated muscles following combined local alpha- and beta-adrenergic blockade (Condition 4), and (v) intact muscles with aortic pressure maintained constant (Condition 5). In Series 2, nicotine was infused directly into the gracilis artery at a rate of 3.6 micrograms/kg/min. Muscle blood flow was obtained with an electromagnetic flowmeter and used to calculate vascular resistance and oxygen consumption (Fick equation). Plasma catecholamine levels were determined with a radioenzymatic method. Intravenous nicotine doubled mean aortic pressure under Conditions 1-4. In intact and denervated muscles (Conditions 1 and 2) proportional increases in vascular resistance, reflective of vasoconstriction, held blood flow constant. Muscle oxygen consumption was unchanged. alpha-Adrenergic blockade with phenoxybenzamine following denervation (Condition 3) converted muscle vasoconstriction to vasodilation during nicotine infusion. Additional beta-adrenergic blockade (Condition 4) restored muscle vasoconstriction. Nicotine-induced muscle vasoconstriction was maintained under controlled pressure (Condition 5). Intravenous nicotine significantly increased plasma catecholamine levels. Intra-arterial infusions of nicotine (Series 2) caused no hemodynamic changes in muscle. In conclusion, intravenous nicotine caused vasoconstriction in muscle, which was not due to reduced metabolic demand, pressure-flow autoregulation, or a direct [corrected] effect on vascular smooth muscle, but to stimulation of alpha-adrenergic receptors. Following denervation, this vasoconstriction was maintained by elevated plasma catecholamines. alpha-Adrenergic blockade unmasked nicotine-induced vasodilation mediated by beta-adrenergic receptors, whereas combined alpha- and beta-adrenergic blockade unmasked nicotine-induced vasoconstriction by a nonadrenergic mechanism.

Adrenergic alpha-Antagonists↗
PubMed2002

A specific force deficit exists in skeletal muscle after partial denervation.

Skeletal muscle demonstrates a specific force deficit after repair of injured peripheral nerves, microneurovascular muscle transfer, and normal aging. Because atrophy cannot account for deficits in specific force, other, unknown, mechanisms are responsible for the resulting muscle contractile dysfunction under these circumstances. We tested the hypothesis that a subpopulation of denervated fibers is partially or completely responsible for the specific force deficit after partial denervation of the rat extensor digitorum longus muscle (EDL). Adult Fisher rats underwent either sham exposure or partial transection of 80% of the cross-sectional area of the left deep peroneal nerve. After a 2-week recovery period, maximum isometric force (F(0)) was measured in situ and maximum specific force (sF(0)) was calculated for EDL from both control (n = 8) and partial denervation (n = 7) groups. Innervated fiber cross-sectional area (CSA(inn)) was measured directly from whole EDL cross sections after immunohistochemical labeling for neural cell adhesion molecule (NCAM), a marker of muscle fiber denervation. A corrected specific force value (sF(0-inn)) was calculated by normalizing F(0) to CSA(inn). Partial skeletal muscle denervation resulted in significant reductions in muscle mass, F(0), and sF(0). The percentage of muscle fibers expressing NCAM in the extrajunctional sarcolemma increased from 1.0 +/- 0.8% in control to 49 +/- 15% in partially denervated EDL muscles. A 62.7% deficit in EDL specific force was observed after partial denervation. Denervated muscle fibers accounted for 59.3% of this deficit, but sF(0-inn) still differed significantly between control and partially denervated muscles, with a 25.5% difference between groups. In partially denervated muscles, the specific force deficit is partially but not fully explained by a subpopulation of noncontractile, denervated fibers.

Animals↗
PubMed1983

Trophic action of nerve extract on denervated skeletal muscle in vivo: dose dependency, species specificity, and timing of treatment.

Atrophy in a denervated muscle results from the disuse caused by paralysis of the muscle, and from the loss of special neurotrophic substances. Proteins extracted from rats' sciatic nerves have been shown to prevent the nondisuse atrophy of denervated rats' extensor digitorum longus (EDL) muscles when administered by intramuscular injection. The present investigation elicited more information about this neurotrophic phenomenon. Extract of liver failed to affect the rate of atrophy of denervated EDL muscles. Injection of various doses of extract of rats' or sheep's sciatic nerves indicated that the action of the extract was dose-dependent but not species-specific. Muscles denervated for 14 days and injected with extract on all 14 days or only on the first or last 7 days all exhibited significantly less atrophy than those that were not injected.

Animals↗
PubMed2004

Inactivity-induced modulation of Hsp20 and Hsp25 content in rat hindlimb muscles.

Denervation decreases small heat shock protein (HSP) content in the rat soleus muscle; however, it is unknown whether this change is due to inactivity or absence of a nerve-muscle connection. Spinal cord isolation (SI) is a model of inactivity with an intact neuromuscular connection. After 7 days of SI, Hsp20 and Hsp25 levels in the soleus, plantaris, and adductor longus muscles were lower than in control rats, whereas Hsp20 was unchanged and Hsp25 increased in the tibialis anterior. The results for the soleus indicate that these small HSPs respond to inactivity and that this response is not influenced by neural activity-independent factors. Furthermore, the data indicate that these HSPs are impacted to a greater degree in muscles that are predominantly slow or have an antigravity function than in flexor muscles. Understanding the regulation of these HSPs during chronic reductions in neuromuscular activity may have valuable applications for conditions such as spinal cord injury.

Animals↗
PubMedDate not supplied

Uptake of horseradish peroxidase in denervated skeletal muscle occurs primarily at the endplate region.

The spatial distribution of horseradish peroxidase (HRP) uptake has been studied by light- and electron microscopy in the denervated hemidiaphragm of the mouse. Segments with high HRP uptake were observed in a band centrally located in the denervated muscle. This distribution is similar to the well-known innervation pattern of the diaphragm. Ultrastructural studies demonstrated a high incidence of postsynaptic folds in close proximity of fibre areas with high intracellular content of HRP. 8-12 days after denervation a large number of fibres showed segments of high HRP uptake. 2-4 days after denervation very few such segments were observed. Biochemical studies also demonstrated an increase in HRP uptake after denervation occurring primarily in the endplate region. The activities of the lysosomal enzymes N-acetyl-beta-D-glucosaminidase, acid phosphatase and cathepsin D all increased after denervation, most prominently in the endplate region. It is suggested that the observed segmental uptake of HRP and lysosomal activation reflects a process for rapid membrane turnover in denervated muscle.

Acetylglucosaminidase↗
PubMed2002

Protective effects of ciliary neurotrophic factor on denervated skeletal muscle.

To study the effects of ciliary neurotrophic factor (CNTF) on denervated skeletal muscle atrophy and to find a new approach to ameliorate atrophy of denervated muscle, a model was established by cutting the right sciatic nerve in 36 Wistar mice, with the left side serving as control. Then they were divided into two groups randomly. CNTF (1 U/ml) 0.1 ml was injected into the right tibial muscle every day in experimental group, and saline was used into another group for comparison. The muscle wet weight, muscle total protein, Ca2+, physiological response and morphology were analyzed on the 7th, 14th and 28th day after operation. Our results showed that compared to control group, there was a significant increase in muscle wet weight, total protein, Ca2+, muscle fiber cross-section area in CNTF group (P < 0.05). CNTF could ameliorate the decrease of tetanic tension (PO), post-tetanic twitch potentiation (PTP), and the prolonged muscle relaxation time (RT) caused by denervation (P < 0.05). The motor end-plate areas 7 days and 14 days after denervation was similar (P > 0.05), but significantly larger 28 days after the denervation (P < 0.05). Our results suggest that CNTF exerts myotrophic effects by attenuating the morphological and functional changes associated with denervation of rat muscles and has protective effects on denervated muscle and motor end plate.

Animals↗
PubMed1975

Influence of activity on the passive electrical properties of denervated soleus muscle fibres in the rat.

The technique of direct electrical stimulation of denervated muscle was used to study the role of muscle activity per se in controlling the passive electrical properties of muscle fibres. 2. Specific membrane resistance and capacitance of the denervated and the denervated-stimulated muscle fibres were measured by a sinewave technique at frequencies between 5 and 240 Hz. The parameter values were constant at low frequencies up to a variable transition frequency and declined rapidly at higher frequencies. 3. Following denervation the low-frequency value of specific membrane resistance increased (2291 omega cm2 for 19-day denervated fibres vs. 766 omega cm2 for innervated fibres), the specific membrane capacitance declined (2-7 muF/cm2 vs. 3-6 muF/cm2) and the transition frequency shifted towards lower frequencies. The specific internal resistance was higher in denervated fibres (301 omega cm for 19-day denervated fibres vs. 240 omega cm in innervated fibres) apart from a transient decline after 5 days of denervation (164 omega cm). 4. Direct electrical stimulation for 2 weeks beginning on the 5th day after denervation restored all parameters listed above to their original values before denervation. 5. Stimulation arrested in most cases further atrophy from the time of stimulation but did not restore normal fibre size.

Animals↗
PubMed1996

Rhodamine B, a fluorescent probe for acidic organelles in denervated skeletal muscle.

We describe a very efficient method for fluorescent labeling of acidic structures in denervated skeletal muscle with rhodamine B. Rhodamine B at 50 ng/ml gave selective and distinct segmental labeling of denervated muscle fibers after 5-min incubation at room temperature. Labeling was also achieved at 4 degrees C. The labeling was disrupted by the ionophores monensin and nigericin, suggesting a labeling confined to acidic structures. Rhodamine B co-localized with the lysosomotropic dye Lyso Tracker Green and a marker for endocytosis (fluorescein isothiocyanate-labeled dextran). Rhodamine B, which is highly lipophilic, showed pH-dependent fluorescence emission in saturated aqueous N-octanol. Tetramethylrhodamine showed similar characteristics for labeling of denervated muscle fibers and pH-dependent fluorescence in N-octanol. The carboxyl group present in these two compounds appears important, because structurally related compounds that either lack this group or have it esterified failed to label denervated muscle fibers and showed no pH-dependent fluorescence in N-octanol. The results suggest that rhodamine B labels acidic organelles belonging to the endosomal/lyosomal system of denervated skeletal muscle fibers. Nevertheless, it failed to label such organelles in a number of mammalian cell types other than denervated skeletal muscle fibers.

Animals↗
PubMed1989

The action of the beta-agonist clenbuterol on protein metabolism in innervated and denervated phasic muscles.

1. Clenbuterol treatment in innervated and denervated phasic extensor digitorum longus, plantaris and gastrocnemius muscles from rats caused a significant increase in RNA and protein contents in all muscles except denervated extensor digitorum longus. 2. All muscles showed an increase in the fractional rate of protein synthesis (Ks) with clenbuterol, but the temporal response varied. 3. The data suggest that the effect of clenbuterol on protein metabolism in innervated muscles is muscle-type specific, and demonstrate the homology of response for denervated muscles.

Animals↗