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At least 919 records · Page 51Linked to original sources
PubMed1978

Glutamate sensitivity and distribution of receptors along normal and denervated locust muscle fibres.

1. Factors influencing the glutamate sensitivity of extrajunctional regions of innervated and denervated locust muscle fibres have been investigated. Properties of the two types of extrajunctional glutamate receptors, D- and H-receptors, have been studied in regions of high and low sensitivity. 2. The low level of extrajunctional sensitivity which is normally present in innervated fibres was 20-30 times higher at the muscle-tendon junction than at other sites; increased sensitivity extended about 20-40 micron from the tendon. After denervation or localized damage the entire extrajunctional sensitivity was increased approximately 100 times above control levels. 3. Applying L-glutamate (which activates D- and H-receptors) and DL-ibotenate (which activates H-receptors) from multibarrelled micropipettes showed that increased extrajunctional sensitivity resulted from an increase in D-receptors while H-receptors were apparently unchanged. 4. Coulomb dose vs. response relationships for the action of glutamate on D-receptors were similar when obtained at the muscle-tendon junction and nerve-muscle junction of innervated fibres or at extrajunctional regions in denervated fibres. 5. Time course of onset and percentage desensitization of D- and H-receptors in innervated fibres were similar. The percentage desensitization of D-receptors in extrajunctional regions of high sensitivity was greatly reduced. 6. It is suggested that D- and H-receptors are independent and that the trigger for increased receptor sensitivity acts specifically on D-receptors. In all respects so far studied, the D-receptors resemble extrajunctional ACh-receptors in vertebrate muscle.

Animals↗
PubMedDate not supplied

[Circular dichroism of actin from denervated skeletal muscles].

Method of circular dichroism did not indicate any changes of the secondary structure of globular and fibrillar actin from denervated skeletal muscles. The matter that some conformational changes of the aromatic residues do in fact accompany denervation was confirmed by fluorescence studies but not by CD spectra.

Actins↗
PubMed1989

Effect of temperature on the maximum rate of rise of tension in denervated rat diaphragm muscle.

Effects of chronic denervation and temperature were studied on the maximum rate of rise of tension in isometric twitch and tetanus of rat diaphragm muscles. The muscles were denervated for 15-20 days and the maximum rate of rise of tension was measured according to Hill (1951). The results showed that the maximum rate of rise of tension in twitch and tetanus was temperature dependent, exponentially increasing with increasing temperatures in both the normal and denervated muscles. A further observation was that the maximum rate of rise of tension in denervated muscle was always smaller than normal controls. It is suggested that probable changes in the series elasticity and duration of active state in the denervated muscle are responsible for the observed changes.

Journal Article↗
PubMed2026

The miR-206-3p/Cpeb1 axis delays acetylcholine receptor degradation and preserves neuromuscular junction stability in denervation-induced muscle atrophy.

Peripheral nerve injury leads to progressive neuromuscular junction (NMJ) destabilization and acetylcholine receptor (AChR) degradation, which are critical drivers of denervation-induced muscle atrophy and impaired motor recovery. However, the post-transcriptional mechanisms regulating AChR stability during denervation remain poorly understood. Here, we investigated the role of miR-206-3p in NMJ maintenance and muscle preservation after denervation, with a focus on its interaction with the RNA-binding protein cytoplasmic polyadenylation element binding protein 1 (Cpeb1). Using C2C12 myoblasts and a sciatic nerve transection mouse model, we demonstrate that miR-206-3p promotes myogenic differentiation, enhances AChR clustering, and preserves postsynaptic AChR morphology. miR-206-3p directly targets the 3' untranslated region of Cpeb1, suppressing its expression, as confirmed by dual-luciferase reporter assays. In vivo, adeno-associated virus-mediated overexpression of miR-206-3p delayed denervation-induced AChR fragmentation, attenuated muscle atrophy, and significantly improved motor function recovery. Conversely, Cpeb1 overexpression accelerated AChR degradation and muscle wasting, whereas co-overexpression of miR-206-3p mitigated these detrimental effects, indicating that Cpeb1 is a key downstream effector of miR-206-3p. Collectively, our findings identify the miR-206-3p/Cpeb1 axis as a previously unrecognized regulator of NMJ stability and muscle integrity after denervation, providing mechanistic insight and a potential therapeutic target for preserving neuromuscular function during prolonged denervation.

Animals↗
PubMed1998

Recovery of rat skeletal muscles after partial denervation is enhanced by treatment with nifedipine.

Following partial denervation of adult rat skeletal muscle intact axons sprout to reinnervate denervated muscle fibres and increase their territory. The extent of this increase is limited and may depend on the ability of axon terminals to form and maintain synaptic contacts with the denervated muscle fibres. Here we tested the possibility whether reducing Ca2+ entry into presynaptic nerve terminals through dihydropyridine sensitive channels may allow more nerve-muscle contacts to be formed and maintained. Hindlimb muscles of adult Wistar rats were partially denervated by removing a small segment of the L4 or L5 spinal nerve on one side. A nifedipine-containing silastic rubber strip was subsequently implanted close to the partially denervated soleus or extensor digitorum longus (EDL) muscles in some animals. In control experiments silastic strips which did not contain nifedipine were used. Several weeks later isometric contractions were recorded, to determine the effect of (a) partial denervation and (b) nifedipine treatment on force output and motor unit numbers. The tension produced by nifedipine treated partially denervated muscles was 82% and 79% of the unoperated contralateral value for soleus and EDL, respectively. This was significantly greater than in untreated muscles, which only produced 61% and 48%, respectively. Mean motor unit force was also significantly larger with nifedipine treatment. Histological analysis revealed that a significantly larger proportion of the total number of muscle fibres remained in nifedipine-treated partially denervated muscles (soleus, 90% and EDL, 101%) compared with untreated muscles (soleus, 51% and EDL, 66%). Thus the number of neuromuscular contacts was increased with nifedipine treatment.

Animals↗
PubMed2001

Calpain 3 mRNA expression in mice after denervation and during muscle regeneration.

Lack of functional calpain 3 in humans is a cause of limb girdle muscular dystrophy, but the function(s) of calpain 3 remain(s) unknown. Special muscle conditions in which calpain 3 is downregulated could yield valuable clues to the understanding of its function(s). We monitored calpain 3 mRNA amounts by quantitative RT-PCR and compared them with those of alpha-skeletal actin mRNA in mouse leg muscles for different types of denervation and muscle injury. Intact muscle denervation reduced calpain 3 mRNA expression by a factor of 5 to 10, while alpha-skeletal actin mRNA was reduced in a slower and less extensive manner. Muscle injury (denervation-devascularization), which leads to muscle degeneration and regeneration, induced a 20-fold decrease in the mRNA level of both calpain 3 and alpha-skeletal actin. Furthermore, whereas in normal muscle and intact denervated muscle, the full-length transcript is the major calpain 3 mRNA, in injured muscle, isoforms lacking exon 6 are predominant during the early regeneration process. These data suggest that muscle condition determines the specific calpain 3 isoform pattern of expression and that calpain 3 expression is downregulated by denervation.

Actins↗
PubMed1998

Expression of specific white adipose tissue genes in denervation-induced skeletal muscle fatty degeneration.

Denervation of skeletal muscle results in rapid atrophy with loss of contractile mass and/or progressive degeneration of muscle fibers which are replaced to a greater or lesser degree by connective and fatty tissues. In this study, we show that denervated rabbit muscles are transformed into a white adipose tissue, depending on their fiber types. This tissue does express LPL, G3PDH and particularly the ob gene, a white adipose tissue-specific marker, and does not express the brown adipose tissue molecular marker UCP1 mRNA.

Adipose Tissue↗
PubMed1977

Effect of nerve length and temperature on the induction of action potentials in denervated slow muscle fibres of the frog.

A. Pyriformis and extensor longus digiti IV muscles of Rana temporaria were denervated by cutting the sciatic or peroneal nerve at various distances from the muscles. Slow fibres were identified by their membrane time constants, and examined for their ability to produce action potentials in response to intracellularly applied current pulses. B. The slow muscle fibres acquired the ability to generate action potentials several days after denervation. The duration of this latent period depended on the length of the peripheral nerve stump, and on the temperature at which the frogs were kept after the operation. C. At 18 degrees C the latent period increased by 0.36 days per mm of sciatic nerve stump. At 11.5 degrees C the corresponding value was 0.7 days/mm. The effect of length of the peroneal nerve was smaller than that of the sciatic nerve. D. It is suggested that the peripheral nerve stump serves as a reservoir of 'trophic' material which is transported towards the slow fibres at a rate of 2.8 mm/day (at 18 degrees C) and seems to block the formation of Na channels. The Q10 value of this transport system would be 2.7.

Action Potentials↗
PubMed1979

Synapse formation in intact innervated cutaneous-pectoris muscles of the frog following denervation of the opposite muscle.

1. Denervation of one cutaneous-pectoris muscle of the frog induces the formation of new synapses in the intact innervated muscle on the opposite side. After crushing the motor nerve to the left muscle the incidence of polyneuronal innervation in the right intact muscle increased from an average normal value of 16% to an average value of 27% (Rotshenker & McMahan, 1976).2. The formation of the new synapses in the intact muscle is independent of the presence of denervated muscle fibres or degenerating axons peripheral to the site of axotomy. After removing the left cutaneous-pectoris muscle, the proportion of polyneuronally innervated muscle fibres in the right intact muscle increased to an average value of 34%.3. The number of new synapses formed in one muscle is dependent upon the type of the lesion to the motor nerve to the opposite muscle; 40% of the muscle fibres on the right side were found to be polyneuronally innervated after transecting the motor nerve on the opposite side, as compared to 27% after crushing it.4. The delay with which new synapses are formed on the unoperated side is dependent upon the distance from the spinal cord of the axotomy. New synapses were detected 4-8 weeks after cutting the opposite nerve close to the muscle. Placing the site of axotomy close to the spinal cord shortened the delay and new synapses were detected as early as 9 days after the operation.5. The stimulus for the formation of new synapses by an intact nerve is ineffective if the injured nerve on the contralateral side originates from distant segments of the spinal cord. The pattern of innervation in cutaneous-pectoris muscles was not altered following denervation of distant muscles in the hind limb.6. These results suggest that the signal for sprouting and synapse formation may arise in the damaged nerve cells, central to the site of axotomy, and then be communicated transneuronally within the spinal cord to the intact motoneurones on the opposite side.

Animals↗
PubMed2006

Activity-dependent gene regulation in skeletal muscle is mediated by a histone deacetylase (HDAC)-Dach2-myogenin signal transduction cascade.

Muscle activity contributes to muscle development and function largely by means of regulated gene expression. Many genes crucial to neuromuscular synapse formation, such as MuSK and nAChRs, are induced before muscle innervation or after muscle denervation, and this induction requires expression of the E-box binding, basic helix-loop-helix muscle-specific transcription factor, myogenin (Mgn). The mechanism by which muscle activity is coupled to gene expression is poorly defined. Here we report that inhibition of histone deacetylase (HDAC) activity attenuates the induction of activity-regulated genes in aneural myotubes and adult denervated muscle. The effect of HDAC inhibitors requires new protein synthesis, suggesting HDACs may regulate the expression of a Mgn transcriptional repressor. We identified Dach2 as a Mgn transcriptional repressor whose expression is dramatically reduced in an HDAC-dependent manner in developing aneural myotubes or adult denervated muscle. Dach2 overexpression in denervated muscle suppressed Mgn, nAChR, and MuSK gene induction, whereas Dach2 knockdown induced Mgn gene expression in innervated muscle and relieved Mgn promoter inhibition by HDAC inhibitors. Thus, a HDAC-Dach2-myogenin signaling pathway has been identified to decode nerve activity and control muscle gene expression in developing and adult skeletal muscle.

Animals↗
PubMed1988

Structural alterations in the membrane of the slow muscle fiber of Rana temporaria after denervation.

Mixed fiber bundles as well as separated slow and fast fibers from normal and denervated muscles of Rana temporaria were freeze-fractured. The membranes of both fiber types are distinguished in this species by the presence of fairly regularly distributed particle aggregates or arrays of different shapes and sizes; the number per unit area of the membrane is six times higher in fast than in slow fibers. The intramembrane particle (IMP) density is higher in slow than in fast fibers. After denervation, the fast fiber membrane structure does not change whereas the slow fiber membrane acquires the characteristics of the fast fiber, i.e., an increase in the density of particle arrays and a decrease in IMP density. These changes in the slow fiber membrane are compared to the altered physiological properties of this fiber type after denervation.

Animals↗
PubMed1988

Immunological evidence for a change in subunits of the acetylcholine receptor in developing and denervated rat muscle.

We used specific antibodies to gamma, delta, and epsilon subunits to characterize acetylcholine receptor (AChR) in extracts and at endplates of developing, adult, and denervated rat muscle. The AChRs in normal adult muscle were immunoprecipitated by anti-epsilon and anti-delta, but not by anti-gamma antibodies, whereas AChRs in denervated and embryonic muscles were precipitated by anti-gamma and anti-delta, but showed little or no reactivity to anti-epsilon antibodies. In immunofluorescence experiments, AChRs at neonatal endplates bound antibodies to gamma or delta, but not epsilon, subunit, whereas those in adult muscles bound antibodies to epsilon or delta, but not gamma, subunit. AChRs at denervated endplates and at developing endplates between postnatal days 9 and 16 bound all three antibodies. We conclude that the distribution of gamma and epsilon subunits of the AChR parallels the distribution of AChRs with embryonic and adult channel properties, respectively.

Animals↗
PubMed1991

Delayed response to denervation in muscles of C57BL/Ola mice.

Muscle fibre areas and numbers, tetanic force, resident macrophage numbers and acetylcholine sensitivity were measured in normal and denervated soleus muscles of C57BL/Ola mice for comparison with data from outbred and other inbred strains. Serum creatine kinase levels were also measured. The muscles of normal C57BL/Ola mice had more fibres, generated more tension, had fewer resident macrophages and had a lower acetylcholine sensitivity than muscles of other strains. The normal level of serum creatine kinase was lower in C57BL/Ola mice than in Balb/c mice. Following denervation, the mean cross-sectional area of muscle fibres in Balb/c mice started to fall from day 1 but a fall was not seen in muscles from C57BL/Ola mice until day 5. The development of increased acetylcholine sensitivity was slower in the C57BL/Ola mice although the values in all mouse strains had converged by five days. The levels of serum creatine kinase also rose more slowly following denervation in C57BL/Ola mice. The differences between the data from C57BL/Ola mice and others are ascribed to the slow rate of Wallerian degeneration in that strain. The results support the view that the effects of denervation on muscle are due to both inactivity and an inflammatory effect contributed by nerve degeneration. The mutation that causes slow nerve degeneration may, however, also affect muscle directly, making it more resistant to catabolism.

Acetylcholine↗
PubMedDate not supplied

[Activity of valyl-tRNA-synthetase and alanyl-tRNA-synthetase in intact and denervated rabbit muscles].

The rate of acylation of non-fractionated tRNA from baker yeast and beef liver with valine-I-C14 and alanine-I-C14 had been measured. The yeast tRNA was found to be the active acceptor of valine while the beef tRNA intensively accepted alanine. The specific activities of valyl- and alanyl-tRNA synthetases from intact m. soleus (red) when measured with yeast tRNA were 4.3 and 3.3 times higher than the activities of the respective enzymes from intact m. gastrocnemius (mixed). 30 days after sciatic nerve section the activities of both aminoacyl-tRNA synthetases in denervated red and mixed muscles had become nearly equal. Equalization of aminoacyl-tRNA synthetases specific activities in the denervated muscles occured as a result of the changes in the catalytic properties and, possibly, in the intracellular concentration of the enzymes.

Alanine-tRNA Ligase↗
PubMed1996

Up-regulation of leukaemia inhibitory factor and interleukin-6 in transected sciatic nerve and muscle following denervation.

Leukaemia inhibitory factor (LIF) and Interleukin-6 (IL-6) are multifunctional cytokines that are related on the basis of their predicted structural similarities and shared signal transducing receptor components. Both these factors stimulate myoblast proliferation, and whereas LIF is neurotrophic for sensory neurons, and for the motor neurons which innervate muscle, IL-6 has only been reported to act on a population of septal neurons in the brain. We have looked at the effect of peripheral nerve trauma on the expression of these factors. We show here that whereas LIF and IL-6 mRNAs are expressed in low levels in normal sciatic nerve and skeletal muscle, there is significant up-regulation in the nerve segments after injury, with proximally and distally. There is also an increase in LIF and IL-6 expression in the denervated muscle located largely in the muscle cells. In addition, while there is retrograde axonal transport of LIF by the sciatic nerve, IL-6 is not retrogradely transported, and as a result, IL-6 does not stimulate the survival of sensory neurons in vitro. Both growth factors are produced by Schwann cells. These results show a rapid response in the expression of these genes after injury and suggest that LIF and IL-6 act as trauma factors but with different roles in injured peripheral nerve.

Animals↗