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PubMed1983

Formation of neuromuscular junctions in transplanted peroneus longus muscles in the rat. A quantitative comparison with reinnervation of the muscle in situ.

The formation of neuromuscular junctions in free heterotopic muscle transplants in the rat has been studied quantitatively and compared with the reinnervation of the muscle in situ. The AChE-containing area and the nerve terminal were stained in the same longitudinal section and the length of end-plate, the average number of nerve terminal branch points within the end-plate and the terminal innervation ratio (TIR) were determined. In denervated muscles we noticed early disappearance of nerves whereas the AChE-stained end-plates were visible after eight weeks. The reinnervation of the muscle in situ and after transplantation showed considerable similarities. Early during reinnervation the number of AChE positive areas increased and many of them were innervated by more than one axon. Terminal axons were also seen innervating more than one end-plate situated on the same or on different muscle fibres. Later the number of end-plates decreased and they were innervated by only one axon. The end-plate length reached normal value in the reinnervated muscle in situ but remained smaller in the transplanted muscle. In all reinnervated muscles ultraterminal sprouting was found as indicated by an increased number of nerve terminal branch points within the end-plate area. The TIR was increased in all reinnervated muscles due to terminal and ultraterminal sprouting of the axon. No significant difference in reinnervation was noted between normal and predenervated transplants. The reinnervation of transplanted muscles obviously has similarities not only with the reinnervation of normal muscles but also with the development of muscular innervation during early postnatal growth. In spite of the plasticity of the peripheral nerve the transplanted muscles underwent considerable atrophy which may have been enhanced by the unphysiological placement of the muscles in the abdomen. However, this experimental model made it possible to study reinnervation of muscle fibres only originating from the graft.

Animals↗
PubMed2004

[Age-related excitability of the muscle after the sciatic nerve blockade in rats].

In adult (8 weeks) and old (24 weeks) white rats early postdenervation changes (in 12 and 24 hours after nerves squeezing) of bioelectric activity of gastrocnemius muscles were studied using electrophysiological methods. Parameters of the activity were: a threshold, chronaxy during direct and indirect muscle irritation; amplitude, duration, the latent period of action potential (AP), an amplitude of AP during increasing stimulation and during dual irritations. It is established that the changes in these parameters in group of adult animals are considerably more pronounced and directed to the increase in excitability of the denervated muscle. In the group of old animals these changes were absent or they were considerably smaller. It is suggested that the cause of more pronounced postdenervated changes in adult animals is a higher speed of axoplasmic transport of the substances in the motor fibers of a isciatic nerve.

Action Potentials↗
PubMed1990

The effect of muscle activity on motor unit size in partially denervated rat soleus muscles.

It has been shown previously that after section of L5 ventral ramus at 5 days the intact axons of L4 ventral ramus retain their large neonatal peripheral field in the rat soleus muscles. Soleus muscles of 5-day-old rats were partially denervated by section of their major neural input, L5 ventral ramus, and in addition paralysed with alpha-bungarotoxin for 3-5 days. The motor unit size was examined 2 months later. The tension developed by individual motor units from muscles that were partially denervated and in addition temporarily paralysed was much less than that after partial denervation alone. This reduced tension output was not due to muscle atrophy but to a smaller number of muscle fibres supplied by individual axons. Thus, unlike after partial denervation only, motoneurons were unable to maintain their large neonatal territory when the muscle was temporarily paralysed and they were unable to reoccupy this territory after the muscles recovered from the paralysis. The possibility that arrested muscle maturation due to paralysis has a permanent effect on motor unit size is discussed.

Animals↗
PubMed1989

Experimental study of vascularized muscle: multifactorial analysis of muscle regeneration following denervation.

An experimental study on regeneration of vascularized muscles after denervation was carried out on a total of 73 adult rat gastrocnemius muscles. A vascularized muscle graft harvested from the gluteal region was transplanted orthotopically with its vascular pedicle. A transected motor nerve of the graft was sutured under the operating microscope. The rats were sacrificed at intervals throughout 12 postoperative months, and biopsied muscles were processed for histologic, immunohistochemical, and composing protein analysis studies. After degeneration of the originally transplanted muscle fibers, regenerating cells such as myoblasts and myotubes developed into mature muscle fibers up to week 8 after surgery. These results suggest that in the regenerating mechanism of vascularized muscle grafts, there are both degenerating and regenerating processes in the transplanted muscles.

Animals↗
PubMed1988

Effect of nerve section on beta-endorphin and alpha-melanotropin immunoreactivity in motor nerves of normal and dystrophic mice.

beta-Endorphin and alpha-melanotropin immunoreactivity was demonstrated in some motor nerves in histological sections of soleus and extensor digitorum longus muscles of the mouse. In two strains (C57BL/6J and 129/ReJ) which can inherit muscular dystrophy, the proportion of immunoreactive nerves was greater in the dystrophic individuals than in their healthy littermates. At 24 h after section of the sciatic nerve in the normal mice the proportion of immunoreactive nerve profiles had increased significantly in the denervated muscles even though most of the nerve axons had degenerated. Similar increases were also seen in nerves in the unoperated contralateral muscles.

Animals↗
PubMed1987

Muscle acetylcholine receptor biosynthesis. Regulation by transcript availability.

The expression of the muscle nicotinic acetylcholine receptor (AChR) on the cell surface entails a complex biosynthetic pathway, involving the expression and assembly of four subunits. The amount of AChR on the cell surface changes throughout muscle development and upon muscle denervation. We have examined the regulatory role of transcript levels on surface AChR expression by RNA blot analysis. During myogenesis of the fusing mouse muscle cell line C2, which expresses an embryonic type of receptor, changes in the rate of appearance of cell surface AChR have been assayed by 125I-alpha-bungarotoxin binding. The maximal increase in the rate of appearance of cell surface AChR occurs upon cell fusion, closely following the maximal increase in transcript levels for the alpha-, beta-, gamma-, and delta-AChR subunits. AChR alpha-, beta-, gamma-, and delta-subunit gene transcript levels have also been examined in innervated and denervated rat and mouse muscle. Muscle denervation results in an increase of transcripts for all four subunits. However, the amount of beta-subunit transcript in innervated rat skeletal muscle is high relative to the other subunit transcripts, and increases less than the other subunit transcripts upon denervation. Our results indicate that, during myogenesis and upon denervation, the availability of AChR subunit transcripts for translation plays a regulatory role in surface AChR appearance.

Animals↗
PubMed1987

Influence of atrophy on the efficiency of muscle reinnervation.

The effectiveness of motor reinnervation carried out after an interval of 20 days between nerve transection and reimplantation onto a foreign muscle was studied in the rat. Sixty days after reimplantation the compound action potential, the maximal indirect twitch and tetanic tensions, and weight loss were evaluated. The functional data demonstrated an incomplete recovery which differed from the complete functional restoration observed in an acutely denervated muscle reinnervated with a chronically severed nerve. Time-dependent changes induced in the muscle by denervation seem therefore to influence the efficacy of motor reinnervation.

Action Potentials↗
PubMed2002

[Effect of glutamate on membrane potential and volume of the skeletal muscle fibers in rats following NO-synthase inhibition in vivo].

Cross-sectional area (CSA) of muscle fibers incubated in culture medium 199 for 3 hours dramatically increases, whereas resting membrane potential (RMP) decreases compared to "freshly-isolated" muscles. Both glutamate and sodium nitroprusside prevent these changes. MK-801, a specific inhibitor of NMDA-receptors, eliminates protective effects of glutamate on both CSA and RMP. NO-synthase inhibition in vivo promotes an increase of initial CSA and decrease of mean RMP. Under these conditions, effects of glutamate and sodium nitroprusside on CSA and RMP of denervated muscles are less obvious. It has been concluded that synaptic glutamate is able to participate in regulation of RMP and cell volume in muscle fibers through the activation of postsynaptic NMDA-receptors and muscle NO-synthase.

Animals↗
PubMed1976

Effects of cyclic nucleotides on mammalian motor nerve terminals.

This research examined the effects of several cyclic nucleotides on in vivo cat soleus nerves and muscles. The reagents were administered by rapid close intra-arterial injection while electrical activity in single motor axons and contractile activity in the whole muscle were monitored. Cyclic N6-2'-O-dibutyryl adenosine 3',5'-monophosphate (dibutyryl cAMP) initiated bursts of action potentials in unstimulated axons. It also caused the occurrence of stimulus bound repetitive potentials in stimulated axons. It caused the muscle to undergo a series of rapid asynchronous contractions and potentiated the strength of stimulus-evoked contractions. Monobutyryl cAMP produced similar responses, but was less potent than dibutyryl cAMP. cAMP produced only a small, transient depression of neuromuscular transmission. There was no response to dibutyryl cyclic 3',5' guanosine monophosphate or sodium butyrate. None of these reagents affected denervated muscle. The results suggest that cAMP-like materials that can penetrate nerve membranes cause depolarization of motor nerve terminals, prolongation of the depolarization of the terminal initiated by an action potential and release of transmitter.

Animals↗
PubMed1980

The effect of lanthanum ions on acetylcholine in frog muscle.

1. Frog sartorius muscles were treated with an irreversible cholinesterase inhibitor and then incubated in Ringer with 2 mM-LaCl3. The amounts of ACh in the tissue and medium were assayed by mass fragmentography, miniature end-plate potentials (min. e.p.p.s) were recorded and the end-plate was investigated by electron microscopy. 2. Addition of La3+ caused in normal, but not in denervated, muscles a discharge of both min. e.p.p.s and chemically detectable ACh. After 30 min both min. e.p.p.s and ACh release decreased. Between 4 and 5 hr after the addition of La3+ min. e.p.p.s had practically ceased and the rate of ACh release was almost back to that in the absence of La3+. 3. La3+ caused a 50% reduction in the ACh content of the tissue within the first 30 min; thereafter ACh gradually increased to 110% by 5 hr. At this time synaptic vesicles were practically absent in most terminals. The ACh was predominantly located in the end-plate regions of the muscles, before as well as after the incubation with La3+. ACh in end-plate free parts of the muscles was unchanged by La3+. 4. Hemicholinium-3 inhibited the synthesis of ACh in the muscles, but it had almost no influence on La3+-induced ACh release. 5. From these and other results, it is concluded that the ACh released by La3+ originates exclusively from the nerve terminals, that most likely this ACh is released via exocytosis from synaptic vesicles, and that the synthesis of ACh following the release of ACh takes place in the nerve terminals. The results further indicate that in freshly excised muscle the greater part (80-90%) of the ACh contained in the nerve terminals is located in the vesicles.

Acetylcholine↗
PubMed1980

Range of variations in motor unit potentials during reinnervation after traumatic nerve lesions in humans.

Successive stages in the reinnervation of denervated muscle fibers following a complete or partial motor nerve lesion in humans were analyzed with the concentric needle electrode during voluntary contraction. Motor unit potential (MUP) patterns were displayed by coherent EMG, in which the potential triggers an oscilloscope sweep and a digital delay line enables the early part of the MUP to be displayed. After a complete nerve lesion, MUPs showing the response of as few as one to three muscle fibers can be observed. MUPs become highly polyphasic as more muscle fibers are incorporated. Marked latency jitter and intermittent blocking of components as well as the occurrence of linked potentials result in complex patterns that may be confused with a "myopathic" pattern of brief small spikes if conventional observation of free-running sweeps is used alone. After a partial nerve lesion, the healthy motor axons achieve extensive collateral reinnervation of the denervated muscle fibers whereby linked potentials of various latencies are added after the original MUP. Adequate understanding of these characteristic features can help clarify some current issues in electromyography. The mechanisms by which long-latency linked potentials and desynchronized components are produced during remodeling of motor units in the course of regeneration involve a number of factors such as slow conduction along regenerated axon branches, ectopic motor end-plates, insecure neuromuscular transmission, and muscle fiber atrophy.

Adolescent↗
PubMed1978

The effect of vibration on blood flow in skeletal muscle in the rabbit.

1. The blood flow in rabbit gastrocnemius, as measured by photoelectric drop-counter, increased when the muscle was vibrated at frequencies of 22--62 Hz. 2. Blood flow increased rapidly within 1--2 s of the start of vibration, and lasted for the whole time vibration was applied. 3. The increase in blood flow was negatively correlated with the initial blood flow, being greater with lower flows. 4. The magnitude of increase was similar in both innervated and acutely denervated muscles. 5. The arterial blood pressure did not change apart from a very brief fall at the beginning of vibration. Venous pressure rose and, consequently, the perfusion pressure was lower. The increase in blood flow thus indicates a considerable dilatation in the resistance vessels of skeletal muscle.

Animals↗
PubMed1996

Muscle contractile activity modulates GLUT4 protein content in the absence of insulin.

We examined whether muscle contractile activity directly modulates GLUT4 protein content in rat skeletal muscle without the participation of insulin action or via amplified insulin action. To attain this purpose, the effects of increased, by training, or eliminated, by denervation, muscle contractile activity on muscle GLUT4 protein concentration were investigated in severely insulin-deficient diabetic rats. For the first set of experiments, insulin-deficient diabetic rats (induced by injection of 80 mg/kg B.W. streptozotocin) were trained for three weeks by treadmill running (90 min/day, 19 m/min, 10%, 6 days/week). GLUT4 protein concentration in soleus muscle was increased by 48% (p < 0.01) as compared with diabetic sedentary animals. For the second set of experiments, rats were injected with streptozotocin (100 mg/kg). The muscles innervated by the sciatic nerve of one leg were denervated four days after injection of streptozotocin. Three days after denervation, soleus muscles in both legs were excised. Insulin deficiency decreased GLUT4 protein concentration in innervated soleus muscle. In insulin-deficient diabetic rats, denervation also decreased soleus GLUT4 protein concentration by 50% (p < 0.01) as compared with the contralateral innervated muscle. Furthermore, the effects of insulin-deficiency and denervation on GLUT4 protein concentration were additive. These results provide evidence that muscle contractile activity directly modulates skeletal muscle GLUT4 protein concentration independent of insulin action.

Animals↗
PubMed1983

Cholinergic growth factor from skeletal muscle elevated following denervation.

The effect of skeletal muscle extracts upon cholinergic neuron in vitro survival was investigated. All muscle soluble protein extracts elicited survival of neurons above that of neurons alone in culture and were found to be active below a protein concentration of 1.0 mg/ml. However, skeletal muscle which had been previously denervated, was found to contain higher amounts of survival activity than innervated muscle extracts. This elevation of survival activity was greatest within the first 7 days post-denervation, but subsequently declined towards the innervated level.

Animals↗
PubMed1995

Lecithinized superoxide dismutase retards wobbler mouse motoneuron disease.

Gene mutations of Cu/Zn superoxide dismutase (SOD) have been discovered in familial amyotrophic lateral sclerosis (ALS). Oxidative stress also plays a role in the pathogenesis of sporadic ALS. Whether antioxidant therapy is beneficial in this fatal disease is now crucial. We have shown that SOD treatment improves neuromuscular dysfunction and morphological changes in wobbler mouse motoneuron disease. Progressive spinal motor neuronopathy and axonopathy, predominantly in the cervical cord, occur at postnatal age 3-4 weeks, leading to muscle weakness and contracture of the forelimbs in this animal. These motor deficits rapidly increase by postnatal age 6-8 weeks, and then slowly progress. Wobbler mice were given two doses daily of phosphatidyl choline-bound Cu/Zn SOD (PC-SOD, 10(4), 10(5) U/kg) or a vehicle solution by intraperitoneal injection from postnatal 3-4 to postnatal 7-8 weeks of age. PC-SOD treatment attenuated progression of motor dysfunction, prevented denervation muscle atrophy, and delayed degeneration of spinal motoneurons in wobbler mice. This raises the possibility that PC-SOD may have therapeutic potential in human motoneuron disease.

Animals↗
PubMed1982

Transneuronal and peripheral mechanisms for the induction of motor neuron sprouting.

After injury to the nerve to one cutaneous pectoris muscle of the frog, the intact nerve to the contralateral muscle sprouts and forms additional synaptic connections with already innervated muscle fibers. It has been suggested (Rotshenker, S. (1979) J. Physiol. (Lond.) 292: 535-547; Rotshenker, S., and F. Reichert (1980) J. Comp. Neurol. 193: 413-422) that axotomy initiates a signal for sprouting in the injured neurons that is transferred transneuronally across the spinal cord to intact motor neurons. The present study was designed to test the hypothesis that axotomy initiates the signal for sprouting by interfering with some trophic signaling between the injured neurons and denervated muscle. Colchicine therefore was applied to the nerve to the left muscles to inhibit axonal transport on whose integrity trophic interactions depend. Consequently, supernumerary innervation developed in contralateral right intact muscles much the same as after axotom. Surprisingly, axons that were exposed to the drug also sprouted and formed synapses. Furthermore, the sprouting response of axons that were exposed to the drug also was produced in nerve fibers that were separated from their cell bodies. These results suggest two ways in which colchicine may produce sprouting and synapse formation and thereby suggest two mechanisms by which motor neurons may be induced to sprout: (a) transneuronally, by presenting growth stimuli to their cell bodies and central processes in the central nervous system and (b) by presenting growth stimuli to their peripheral extensions.

Animals↗
PubMed1999

Infraterminal spreading and extrajunctional expression of nicotinic acetylcholine receptors in denervated rat skeletal muscle.

Through the use of biotinylated-bungarotoxin and monoclonal antibodies, the nicotinic acetylcholine receptor (nAChR) was localized in the subneural apparatus of mammalian motor end plates of the flexor digitorum brevis muscle of the adult rat at the light and electron microscopic levels. Under normal conditions, nAChR was located in the primary post-synaptic membrane of the neuromuscular junction, and the depths of the junctional folds constituting the secondary post-synaptic membrane did not contain any nAChR. Up to 75 days after repeated transection of the related motor nerve (sciatic), there was no major alteration in the light-microscopic localization of junctional nAChR in the subneural apparatus, except for a moderate shrinkage and increased immunocytochemical reactivity of the subneural apparatus. At the electron microscopic level, however, immunocytochemical reactivity gradually occupied the entire extent of the secondary post-synaptic membrane, including the depths of the junctional folds, which exhibited extensive branching. In non-innervated portions of the muscle fibers, nAChR receptor appeared in a linear localization on the surfaces of denervated muscle fibers. This linear reaction was not continuous with the nAChR reaction of the motor end plates. It is concluded that denervation supersensitivity might not be due to spreading of junctional nAChR from the end-plate area, but rather to expression of nAChR in non-innervated portions of the muscle fiber and to the infraterminal (subsynaptic) spreading of nAChR into the depths of junctional folds.

Animals↗
PubMed2004

Imaging of peripheral nerve lesions.

PURPOSE OF REVIEW: Clinical investigations of peripheral nerve lesions routinely involve nerve conduction studies and electromyography. Imaging studies are often used to exclude focal mass lesions or external compression and to visualize muscle atrophy. More recently, it has been recognized that magnetic resonance imaging can identify changes in peripheral nerves and secondary neurogenic alterations in skeletal muscle, which may significantly enhance its use in the differential diagnosis of peripheral nerve disease. RECENT FINDINGS: Acute axonal nerve lesions cause a hyperintense signal on T2-weighted images at and distal to the lesion site, which correlates with Wallerian degeneration and nerve oedema. Superparamagnetic iron oxide particles provide an exciting new tool to detect the invasion of macrophages into the degenerating nerve distal to an axonal lesion. Prolongation of the T2 relaxation time and gadolinium enhancement of denervated muscle develop in parallel to the development of spontaneous activity on electromyography, and are probably the consequence of capillary enlargement and increased muscular blood volume. SUMMARY: Magnetic resonance imaging supplements the differential diagnosis of peripheral nerve disease. An advantage over clinical neurophysiological investigations is that it is operator independent and painless. It can identify axonal damage and may thus help to identify a lesion site precisely, where fractionated nerve conduction studies are not applicable. Novel contrast media may potentially be used to detect pathophysiologically relevant mechanisms such as infiltration of the nerve by macrophages. Magnetic resonance imaging also has the advantage of providing a lasting detailed topographical picture of regional variations and avoids localization errors of muscles in electromyography.

Humans↗