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PubMed1993

Changes in mitochondrial calmitine and calcium in rat denervated skeletal muscle after injection of a myotoxic drug, chlorpromazine.

1. Calmitine and mitochondrial calcium were studied after injection of chlorpromazine into control and denervated gastrocnemius muscle in rat. 2. Calmitine decreased under the effect of chlorpromazine and then increased again. Regenerative capacity was more marked for denervated than control muscle. Calcium increased and then returned to its normal level in control muscle while remaining elevated in denervated muscle. 3. Thus, it would appear that calmitine synthesis can occur in the absence of innervation and that denervation, which probably causes disturbances in mitochondrial calcium regulation systems, may prevent total regeneration of muscle after an injury.

Animals↗
PubMed1976

The denervated cremaster muscle of the guinea-pig as a pharmacological preparation.

The pharmacological responses of both denervated and innervated cremaster muscle preparations from the guinea-pig have been investigated and compared. Acetylcholine (ACh) dose-response curves were obtained in both preparations. The affinity constants for (+)-tubocurarine and for atropine were calculated and indicated that the ACh receptors in both preparations were nicotinic. Histamine dose-response curves could be obtained only in the denervated preparation. The response was unaltered by metiamide, and the affinity constant for mepyramine fitted in with those previously obtained by others on ileum and trachea, indicating that the histamine receptors are H1 in type. Sustained contractions were obtained to adrenaline and noradrenaline but not isoprenaline, with the denervated preparations. Schultz-Dale responses were obtained with denervated muscle in sensitized guinea-pigs. This preparation did not respond to 5-hydroxytryptamine, bradykinin, or the slow-reacting substance of anaphylaxis.

Acetylcholine↗
PubMed1977

The binding of labelled saxitoxin to the sodium channels in normal and denervated mammalian muscle, and in amphibian muscle.

1. The binding of [3H]saxitoxin to innervated and denervated rat diaphragm muscle, and to normal frog muscle, has been measured. 2. A saturable component of saxitoxin binding, which was inhibited by tetrodotoxin, was detected in all preparations, as well as a component of non-saturable binding. The values for the maximum saturable capacity, M, and the equilibrium binding constant, K, for normal rat diaphragm muscle were: M = 24-4 f-mole.mg wet-1, and K = 3 -8 NM. 3. Denervation of rat diaphragm muscle reduced the maximum binding capacity per unit weight to 16-5 f-mole.mg-1. The value of K remained virtually unchanged at 4-2 nM. 4. It is suggested that the decrease in density per unit weight does not reflect any change in the density of sodium channels per unit area of membrane. 5. Two varieties of the same species of frog, Rana pipiens, were examined. In one variety (Southern) the value of M was 25-6 f-mole.mg-1 and the value of K was 4-3 nM. In the Northern variety the maximum binding capacity was less, M being 14-6 f-mole.mg-1; the value of K was 3-8 nM.

Action Potentials↗
PubMed2001

"Donor" muscle structure and function after end-to-side neurorrhaphy.

End-to-end nerve coaptation is the preferred surgical technique for peripheral nerve reconstruction after injury or tumor extirpation. However, if the proximal nerve stump is not available for primary repair, then end-to-side neurorrhaphy may be a reasonable alternative. Numerous studies have demonstrated the effectiveness of this technique for muscle reinnervation. However, very little information is available regarding the potential adverse sequelae of end-to-side neurorrhaphy on the innervation and function of muscles innervated by the "donor" nerve. End-to-side neurorrhaphy is hypothesized to (1) acutely produce partial donor muscle denervation and (2) chronically produce no structural or functional deficits in muscles innervated by the donor nerve. Adult Lewis rats were allocated to one of two studies to determine the acute (2 weeks) and chronic (6 months) effects of end-to-side neurorrhaphy on donor muscle structure and function. In the acute study, animals underwent either sham exposure of the peroneal nerve (n = 13) or end-to-side neurorrhaphy between the end of the tibial nerve and the side of the peroneal nerve (n = 7). After a 2-week recovery period, isometric force (F(0) was measured, and specific force (sF(0) was calculated for the extensor digitorum longus muscle ("donor" muscle) for each animal. Immunohistochemical staining for neural cell adhesion molecule (NCAM) was performed to identify populations of denervated muscle fibers. In the chronic study, animals underwent either end-to-side neurorrhaphy between the end of the peroneal nerve and the side of the tibial nerve (n = 6) or sham exposure of the tibial nerve with performance of a peroneal nerve end-to-end nerve coaptation approximately 6), to match the period of anterior compartment muscle denervation in the end-to-side neurorrhaphy group. After a 6-month recovery period, contractile properties of the medial gastrocnemius muscle ("donor" muscle) were measured. Acutely, a fivefold increase in the percentage of denervated muscle fibers (1 +/0 0.7 percent to 5.4 +/-2.7 percent) was identified in the donor muscles of the animals with end-to-side neurorrhaphy (p < 0.001). However, no skeletal muscle force deficits were identified in these donor muscles. Chronically, the contractile properties of the medial gastrocnemius muscles were identical in the sham and end-to-side neurorrhaphy groups. These data support our two hypotheses that end-to-side neurorrhaphy causes acute donor muscle denervation, suggesting that there is physical disruption of axons at the time of nerve coaptation. However, end-to-side neurorrhaphy does not affect the long-term structure or function of muscles innervated by the donor nerve.

Anastomosis, Surgical↗
PubMed2005

Use of muscle fibrillation for tracking nerve regeneration.

Individual muscle fibers in denervated muscle demonstrate repetitive, spontaneous contraction. Such fibrillation activity disappears in denervated muscle if reinnervation occurs, but this relationship has not been formally studied. To test whether the disappearance of fibrillation can be used to track nerve regeneration, we quantified the presence and subsequent disappearance of electromyographic (EMG) fibrillation potentials and fibrillation-related movement in the rat tongue after unilateral hypoglossal nerve crush at two locations. In mice, fibrillation movement of vibrissae were monitored after unilateral facial nerve crush and compared with the return of symmetrical vibrissae sweeping movements. In both of these rodent cranial motor systems, there was a conspicuous loss of fibrillation at a time when reinnervation is known to take place, suggesting that the visual appearance of fibrillation-related movement can be used as a simple, noninvasive means of tracking nerve regeneration in these popular experimental motor systems.

Animals↗
PubMed1998

Regulation of glucose transporters GLUT-4 and GLUT-1 gene transcription in denervated skeletal muscle.

Because GLUT-4 expression is decreased whereas GLUT-1 expression is increased in denervated skeletal muscle, we examined the effects of denervation on GLUT-4 and GLUT-1 gene transcription. The right hindlimb skeletal muscle of male transgenic mice containing sequential truncations (2,400, 1,639, 1,154, and 730 bp) of the human GLUT-4 promoter linked to the chloramphenacol acyl transferase (CAT) gene was denervated, and the contralateral hindlimb was sham operated. RNase protection analysis revealed that after 72 h denervation decreased CAT mRNA and GLUT-4 mRNA levels 64-85%, respectively (P < 0.05), in the gastrocnemius muscles. In contrast, denervation of the right hindlimb of male rats increased GLUT-1 gene transcription and GLUT-1 mRNA levels by 94 and 213%, respectively (P < 0.05). In conclusion, GLUT-4 transcription is decreased but GLUT-1 transcription is increased in denervated skeletal muscle, suggesting that the effects of denervation on GLUT-4 and GLUT-1 expression are, in part, transcriptionally mediated. Furthermore, these data indicate that a DNA sequence regulated by denervation is located within 730 bp of the 5'-flanking promoter region of the human GLUT-4 gene.

Animals↗
PubMed1965

ANAPHYLACTIC REACTION OF DENERVATED SKELETAL MUSCLE IN THE GUINEA PIG.

Muscle strips taken from chronically denervated hemidiaphragms of guinea pigs immunized to ovalbumin react in vitro to the administration of small amounts of this protein with a contraction similar to that of visceral muscle in the Schultz-Dale reaction. A sustained shortening is produced by histamine on denervated diaphragmatic muscle from both sensitized and nonsensitized guinea pigs.

Abdominal Muscles↗
PubMed1981

Mechanical properties of tenotomized and denervated-tenotomized muscles.

Mechanical properties of rat soleus and plantaris muscles were studied in vitro following tenotomy, denervation, or tenotomy plus denervation, all of 3 wk duration. Controls included muscles from sham-operated animals and from animals with muscle tendons severed but immediately resutured. Results of twitch times, times to peak tension, and times to half-relaxation for 145 muscles clearly showed that the slight increase in muscle speed that occurs in the soleus muscles only is due to severance of the muscle tendon per se and not related to muscle shortening and possible related alterations in muscle spindle activity that occurs in simple tenotomy. Furthermore, any demonstrable mechanical changes that occur with tenotomy or with section and resuturing of the tendon requires the presence of intact innervation. We conclude that, contrary to published opinion, tenotomy does not transform slow contracting muscles into fast contracting muscles and that comments concerning the role of stretch receptors in this postulated transformation are pure conjecture, unsupported by experimental data.

Animals↗
PubMed1986

Influence of isaxonine on the target phenomenon, muscle fibre size and neuromuscular junction in the tenotomized and denervated gastrocnemius muscle of the rat.

Isaxonine is reported to accelerate the rate of peripheral nerve regeneration, stimulate axonal sprouting and promote motor and sensory function recovery. The target phenomenon in muscle fibers is the morphological expression of increased stretch activity in a diseased muscle. It can be produced in the gastrocnemius muscle of the rat by tenotomy and is inhibited by simultaneous denervation. The influence of isaxonine on this experimental model was studied. Twenty Wistar rats were submitted to bilateral section of the Achilles tendon and section of the left sciatic nerve. In ten rats, treated with isaxonine, the qualitative and quantitative changes in the gastrocnemius muscle were compared with the control group over a period of 3 weeks. No statistical differences were observed in the occurrence and inhibition of the target phenomenon, the muscle fibre size and the neuromuscular junction. Isaxonine has no direct effect on a diseased muscle with an intact nerve supply, nor in the early stages after complete denervation.

Achilles Tendon↗
PubMed1991

Myogenin and MyoD join a family of skeletal muscle genes regulated by electrical activity.

Myogenin and MyoD are proteins that bind to the regulatory regions of a battery of skeletal muscle genes and can activate their transcription during muscle differentiation. We have recently found that both proteins interact with the enhancer of the nicotinic acetylcholine receptor (nAChR) alpha subunit, a gene that is regulated by innervation. This observation prompted us to study if myogenin and MyoD transcript levels are also regulated by skeletal muscle innervation. Using Northern blot analysis, we found that MyoD and myogenin mRNA levels begin to decline at embryonic day 17 and attain adult levels in muscle of newborn and 3-week-old mice, respectively. In contrast, nAChR mRNAs are highest in newborn and 1-week-old mouse muscle and decline thereafter to reach adult levels in 3-week-old mice. To determine if the down-regulation of myogenin and MyoD mRNA levels during development is due to innervation, we quantitated message levels in adult calf muscles after denervation. We found that in denervated muscle myogenin and MyoD mRNAs reach levels that are approximately 40- and 15-fold higher than those found in innervated muscle. Myogenin mRNAs begin to accumulate rapidly between 8 and 16 hr after denervation, and MyoD transcripts levels begin to increase sharply between 16 hr and 1 day after denervation. The increases in myogenin and MyoD mRNA levels precede the rapid accumulation of nAChR alpha-subunit transcripts; receptor mRNAs begin to accumulate significantly after 1 day of denervation. The effects of denervation are specific because skeletal alpha-actin mRNA levels are not affected by denervation. In addition, we found that the repression of myogenin and MyoD expression by innervation is due, at least in part, to "electrical activity." Direct stimulation of soleus muscle with extracellular electrodes repressed the increase of myogenin and MyoD transcripts after denervation by 4- to 3-fold, respectively. In view of these results, it is interesting to speculate that myogenin and/or MyoD may regulate a repertoire of skeletal muscle genes that are down-regulated by electrical activity.

Aging↗
PubMed2004

Muscle magnetic resonance imaging of denervation and reinnervation: correlation with electrophysiology and histology.

A signal increase in denervated muscle on magnetic resonance imaging (MRI) has been described in several clinical and experimental studies. Here, we studied the time course of T2-relaxation time changes in denervation and subsequent reinnervation in a rat model and correlated the findings with electrophysiology and quantitative histology. A prolongation of the T2 relaxation time in muscles was present 48 h after denervation, which was paralleled by spontaneous activity on electromyography (EMG). Histologically, there was a marked enlargement of the capillaries at that time point, indicating increased blood volume. The relaxation time changes peaked 3 weeks after beginning of nerve regeneration identified by EMG. Subsequently, the T2 prolongation normalized until 10 weeks after beginning of regeneration which was associated with a histological regression of the capillary enlargement. MRI closely mirrors the electrophysiological changes following denervation and reinnervation and may thus be used as adjunct to electrophysiology. The pathophysiological basis for the MR relaxation time changes is predominantly the enlargement of the capillary bed.

Animals↗
PubMed1986

Sodium channel kinetics in normal and denervated rabbit muscle membrane.

The effects of chronic denervation on sodium (Na) channels in rabbit muscle membrane were determined using intracellular microelectrodes and Vaseline gap voltage clamp techniques. The Hodgkin-Huxley model was used to describe the kinetic and steady-state parameters of channel activation and fast inactivation. Chronic (7-10 days) denervation was found to cause a decreased resting potential, lowered action potential peak, and fibrillation potentials in rabbit extensor digitorum longus (EDL) muscles. Under voltage clamp conditions, no differences were observed between denervated and normal fibers in the voltage dependence of the steady-state Na channel activation and fast inactivation curves, or in the time course of development of fast inactivation. However, in denervated fibers, the time course of recovery from fast inactivation was approximately half that measured in normal fibers. Also, whereas depolarizing holding potentials induced a long-term inactivation to varying degrees in normal EDL fibers, denervated EDL fibers and normal soleus fibers were uniformly resistant to prolonged depolarization. These results suggest that the denervation-induced development of spontaneous activity may be due in part to changes in the mechanisms that control the refractoriness of Na channels.

Animals↗
PubMed1995

Stabilisation of neuromuscular junctions by leupeptin increases motor unit size in partially denervated rat muscles.

The effect on inhibiting the calcium activated neutral protease (CANP) by leupeptin on force output and motor unit size of the partially denervated rat EDL muscle was studied. Partial denervation was performed under anaesthesia by section of the L4 ventral ramus in 3- and 18-day-old Wistar rats. Two days after the operation a silicon strip containing the inhibitor of CANP leupeptin was implanted alongside the partially denervated EDL. Two to 3 months later the animals were anaesthetized and the EDL muscles on both sides prepared for tension recording. The results from these recordings show dramatic reduction in force output and muscle weight in animals operated at 3 days and this reduction was less pronounced in muscles treated with leupeptin. The mean force output of individual motor units increases in the leupeptin-treated partially denervated muscle compared to the untreated muscle. The increased fatigue resistance typical of muscles partially denervated at 3 days [37] is less pronounced in the treated muscle. In animals operated at 18 days the individual motor units actually increased in size and the leupeptin treatment had no effect on the partially denervated EDL muscles. The difference between the response to leupeptin of the 3 day and 18 day operated animals could be due to the different patterns of innervation of the muscles at the time of the application of the inhibitor of CANP.

Animals↗
PubMed1990

Cardiac troponin T in developing, regenerating and denervated rat skeletal muscle.

Fetal rat skeletal muscles express a troponin T (TnT) isoform similar to the TnT isoform expressed in the embryonic heart with respect to electrophoretic mobility and immunoreactivity with cardiac TnT-specific monoclonal antibodies. Immunoblotting analyses reveal that both the embryonic and the adult isoforms of cardiac TnT are transiently expressed during the neonatal stages. In addition, other TnT species, different from both cardiac TnTs and from the TnT isoforms expressed in adult muscles, are present in skeletal muscles during the first two postnatal weeks. By immunocytochemistry, cardiac TnT is detectable at the somitic stage and throughout embryonic and fetal development, and disappears during the first weeks after birth, persisting exclusively in the bag fibers of the muscle spindles. Cardiac TnT is re-expressed in regenerating muscle fibers following a cold injury and in mature muscle fibers after denervation. Developmental regulation of this TnT variant is not coordinated with that of the embryonic myosin heavy chain with respect to timing of disappearance and cellular distribution. No obligatory correlation between the two proteins is likewise found in regenerating and denervated muscles.

Animals↗