Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Muscle development”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,675 records · Page 93Linked to original sources
PubMed1994

Satellite cells in slow and fast rat muscles differ in respect to acetylcholinesterase regulation mechanisms they convey to their descendant myofibers during regeneration.

The hypothesis of satellite cell diversity in slow and fast mammalian muscles was tested by examining acetylcholinesterase (AChE) regulation in muscles regenerating 1) under conditions of muscle disuse (tenotomy, leg immobilization) in which the pattern of neural stimulation is changed, and 2) after cross-transplantation when the regenerating muscle develops under a foreign neural stimulation pattern. Soleus (SOL) and extensor digitorum longus (EDL) muscles of the rat were allowed to regenerate after ischemic-toxic injury either in their own sites or had been cross-transplanted to the site of the other muscle. Molecular forms of AChE in regenerating muscles were analyzed by velocity sedimentation in linear sucrose gradients. Neither tenotomy nor limb immobilization significantly affected the characteristic pattern of AChE molecular forms in regenerating SOL muscles, suggesting that the neural stimulation pattern is probably not decisive for its induction. During an early phase of regeneration, the general pattern of AChE molecular forms in the cross-transplanted regenerating muscle was predominantly determined by the type of its muscle of origin, and much less by the innervating nerve which exerted only a modest modifying effect. However, alkali-resistant myofibrillar ATPase activity on which the separation of muscle fibers into type I and type II is based, was determined predominantly by the motor nerve innervating the regenerating muscle. Mature regenerated EDL muscles (13 weeks after injury) which had been innervated by the SOL nerve became virtually indistinguishable from the SOL muscles in regard to their pattern of AChE molecular forms. However, AChE patterns of mature regenerated SOL muscles that had been innervated by the EDL nerve still displayed some features of the SOL pattern. In regard to AChE regulation, muscle satellite cells from slow or fast rat muscles convey to their descendant myotubes the information shifting their initial development in the direction of either slow or fast muscle, respectively. The satellite cells in fast or slow muscles are, therefore, intrinsically different. Intrinsic information is expressed mostly during an early phase of regeneration whereas later on the regulatory influence of the motor nerve more or less predominates.

Acetylcholinesterase↗
PubMed1995

Dynamics of nerve-muscle interaction in developing and mature neuromuscular junctions.

Neuromuscular connections have long served as models of synaptic structure and function. They also provide illuminating insights into the dynamic cell-cell interactions governing synaptogenesis, neuromuscular differentiation, and the maintenance of effective function. This paper reviews recent advances in our understanding of the regulatory and inductive interactions involved in motor axon pathfinding, target recognition, bidirectional control of gene expression during synapse formation, motoneuron cell death, terminal rearrangement, and the ongoing remodeling of synaptic number, structure, and function to adjust to growth and changes in use.

Acetylcholinesterase↗
PubMed1984

The genetic specification of pattern in a Drosophila muscle.

During development of Drosophila the bithorax complex of genes is responsible for diversification of segments in the ectoderm. The muscles derive from the mesoderm and their pattern also varies from segment to segment--a variation that could be determined directly through deployment of the bithorax complex in the muscle cells themselves. Alternatively, the muscle pattern could be determined indirectly, either by the epidermal cells to which the muscles attach, or by the nerves which contact developing muscles. Using a segment-specific muscle found only in males and a new mutation in the bithorax complex, we show that the development of this muscle is independent of the sex and segmental identity of the epidermis. The development of the muscle therefore depends on the sex and state of the bithorax complex in the muscle nuclei themselves or in part of the central nervous system.

Abdomen↗
PubMed1992

Effect of low Ca2+ solution on muscle contraction of developing, preclinical dystrophic (dy2j) mice.

EDL muscles from normal and dystrophic (dy2j) mice aged 7 to 21 days of postnatal life were examined. Muscles were divided into 2 groups according to age, 7 to 14 days and 16 to 21 days postnatal, so as to assess age- and/or phenotype-related differences in the muscle response to low Ca2+ solution. Tension production was already much impaired in "predystrophic" muscles. At this stage, however, there was essentially no difference in twitch kinetics between normal and dystrophic muscles. Upon exposure to low Ca2+ solution, twitch responses of both normal and dystrophic muscles declined in a similar manner. In the youngest animals studied (7 to 14 days), the tetanic responses of both normal and dystrophic muscles to low Ca2+ solution were also similar. In animals 15 to 21 days old, however, the tetanic tension developed in low Ca2+ solution by dystrophic muscles, was significantly less than that of normal. Moreover, under these conditions (i.e., in low Ca2+ solution), and following tetanic stimulation, the membrane potential of dystrophic muscles in this age group was significantly more depolarized than that of normal muscles. Our results suggest that the ability of the cell to deal with extracellular Ca2+ is normal in predystrophic muscles up to 21 days of postnatal life. The results also clearly point to the fragility of the membrane in these muscles.

Age Factors↗
PubMed1993

[Anesthetic-induced heart arrest. A case report of 2 infants with previously unrecognized muscular dystrophy].

We report two boys aged 4 and 10 months who suffered cardiac arrests after induction of anaesthesia. Both infants had no personal or family history of myopathy. In both cases anaesthesia was induced by inhalation with halothane and N2O/O2 (70/30). To facilitate tracheal intubation both were given succinylcholine after the administration of atropine. The 4-month-old developed muscle rigidity and cardiac arrest occurred immediately after tracheal intubation. Resuscitation was unsuccessful. Laboratory findings during resuscitation showed elevated serum potassium levels of more than 10 mmol/l and serum creatine phosphokinase 17.700 IU/l. Histopathologic examination of the skeletal muscle revealed congenital muscular dystrophy. In the older boy no muscle contractures were noted after administration of succinylcholine. He developed bradycardia that progressed to asystole 15 min after induction of anaesthesia. After 1 h of resuscitation a sinus rhythm could be established. The boy developed myoglobinuria and his serum creatine phosphokinase reached a maximum level of 45,000 IU/l on the 2nd day. The child survived and made a complete recovery. Two months later a muscle biopsy taken from the quadriceps showed marked muscular dystrophy. Duchenne's muscular dystrophy could be excluded. The most likely underlying reasons for these complications are discussed: anaesthesia-induced acute rhabdomyolysis or malignant hyperthermia.

Anesthesia↗
PubMed2006

Muscle growth and fiber type composition in hind limb muscles during postnatal development in pigs.

Rapid postnatal development in pigs is reflected by differentiation in skeletal muscle. This process depends on muscle function and demands, but a comprehensive overview of individual developmental characteristics of quickly growing leg muscles in pigs is still missing. This study focused on the development of 10 hind limb muscles in pigs. To determine these changes in mass, fiber type patterns and fiber diameters were analyzed 0, 2, 4, 7, 14, 28, 42, 56 and 400 days after birth. Generally, the proportion of slow fibers increased from birth to 8 weeks. Thereafter, only minor changes in muscle fiber type composition were observed. The majority of the muscles contained less then 10% slow-twitch fibers at birth, increasing to between 12 (Musculus vastus lateralis) and 38% (M. gastrocnemius medialis) in adult pigs. By contrast, postural muscles already had 20-30% slow fibers at birth, and this contribution increased up to 65% in adults (i.e. M. vastus intermedius). From birth to the 2nd week, only in slow fibers could activity of oxidative enzymes be detected. A differentiation of fast-twitch fibers into subtypes with high (comparable to type IIA) and low oxidative metabolism (equivalent to type IIB) occurred between the 2nd and 4th week of life. The ratio between type II fibers with high and low oxidative enzyme activity did not change markedly through development in any muscle, although there was a trend towards an increasing proportion of type IIA fibers in the soleus. In the majority of the muscles investigated, the fast-twitch fibers with low oxidative metabolism (IIB) obtained the largest cross-sectional area. In contrast, at birth no remarkable differences in the diameter of fast and slow fibers were found. The rapid increase in muscle mass compared to body mass reflects the high performance in meat production of the cross pig investigated.

Animals↗
PubMed1996

Critical illness myopathy and neuropathy.

BACKGROUND: Critically ill patients may develop muscle weakness or paralysis during the course of sepsis and multiple-organ failure. We studied peripheral nerve and muscle disorders (NMD) in comatose patients. METHOD: Comatose patients who developed paralysis associated with absent deep-tendon reflexes had electroneuromyography (ENMG) and muscle-nerve biopsy specimens taken. Onset and duration of sepsis, multiple-organ dysfunction and failure, biochemical alterations, and drugs potentially interfering with nerve-muscle function were recorded. FINDINGS: 24 patients became quadriparetic or quadriplegic; muscle changes were found in 23. Axonal neuropathy was found in eight of 22 patients examined. All patients had prolonged sepsis and multiple-organ dysfunction, but only 14 had multiple-organ failure. Drugs such as steroids, neuromuscular-blocking agents, and aminoglycosides were not responsible for paresis, and the part played by hyperglycaemia and hypoalbuminaemia is uncertain. Attending physicians predicted a fatal outcome in all cases, although six of seven survivors fully recovered within 115-210 days from the onset of paralysis. INTERPRETATION: Comatose patients may become completely paralysed because of NMD. The diagnosis is important to avoid unnecessary investigations and unreasonably pessimistic prognosis. ENMG is essential for the diagnosis and for planning further clinical management. Biopsy needs to be done only when it is necessary to properly classify NMD.

Biopsy↗
PubMed1980

Acetylcholine sensitivity of developing ectopic nerve-muscle junctions in adult rat soleus muscles.

1. The development of junctional ACh sensitivity has been studied during the formation of ectopic nerve-muscle junctions (n.m.j.s) between the superficial fibular nerve and the denervated soleus muscle of adult rats. 2. When the soleus nerve was cut 2 weeks or more after implanting the fibular nerve, spontaneous m.e.p.p.s and evoked e.p.p.s were first detected in the vicinity of the fibular nerve sprouts 2.5-3 days later. At this time, peaks of local ACh sensitivity greater than the high level of extrajunctional sensitivity induced by denervation were found near the sprouts of the fibular nerve. 3. During the first week of foreign innervation, the extrajunctional sensitivity of the newly innervated muscle fibres fell, but the peaks of sensitivity in the region of the fibular nerve sprouts persisted. Many of these peaks occurred at sites of transmitter release from the fibular nerve terminals. Each innervated fibre had from 1-8 such peaks. 4. When the fibular nerve was cut 2 days or more after cutting the soleus nerve peaks of ACh sensitivity persisted in the region of the degenerated foreign nerve terminals even if the extrajunctional sensitivity was abolished by direct electrical stimulation of the muscle starting soon after cutting the fibular nerve. 5. When the fibular nerve was left intact, more than half of the peaks of sensitivity formed initially in the region of the foreign nerve sprouts had disappeared 2-3 weeks after cutting the soleus nerve. 6. We conclude that during the formation of ectopic n.m.j.s in adult rat muscle the foreign nerve terminals bring about two types of long-lasting change in the distribution and stability of the underlying ACh sensitivity in the muscle fibre membrane; an increase and stabilization of sensitivity at sites of transmitter release which occurs by the time functional transmission at the newly formed n.m.j.s can be detected, and a loss of sensitivity at some of the sites which takes place about 1-2 weeks later.

Acetylcholine↗
PubMed2001

Misexpression of Fgf-4 in the chick limb inhibits myogenesis by down-regulating Frek expression.

Skeletal muscle development involves an initial period of myoblast replication followed by a phase in which some myoblasts continue to proliferate while others undergo terminal differentiation. The latter process involves the permanent cessation of DNA synthesis, activation of muscle-specific gene expression, and fusion of single cells to generate multinucleated muscle fibres. The in vivo signals regulating the progression through all these steps remain unknown. Fibroblast growth factors (Fgfs) and Fgf receptors comprise a large family whose members have been shown to play multiple roles in the development of skeletal muscle in vitro. Exogenously applied Fgfs are able to stimulate proliferation and suppress myogenic differentiation in cell culture. We sought to determine the role played by Fgf-4 during limb myogenesis in vivo. Fgf-4 transcripts are located at both extremities of myotubes whereas the mRNAs of one of the Fgf receptors, Frek, are detected in mononucleated proliferating myoblasts surrounding the multinucleated fibres. Overexpression of mouse Fgf-4 (mFgf-4) using a replication-competent retrovirus, RCAS, leads to a down-regulation of muscle markers followed by an inhibition of terminal differentiation in limb muscles. Using quail/chick transplantations we were able to follow the muscle cells and found a dramatic decrease in their number after exposure to mFgf-4. Interestingly ectopic mFgf-4 down-regulates Frek transcripts in limb muscle areas. We conclude that overexpression of mFgf-4 inhibits myoblast proliferation, probably by down-regulating Frek mRNAs. This suggests a role for Fgf-4, located at the extremities of the myotubes, where it could be responsible for the absence of Frek mRNA in the muscle fibre.

Animals↗
PubMed1992

Expression of NCAM isoforms during skeletal myogenesis in the mouse embryo.

We have examined the developmental patterns of neural cell adhesion molecule (NCAM) gene expression in embryonic mouse skeletal muscle cells by in situ hybridization. Moreover, by utilising exon-specific cRNA probes, we have examined tissue specific splicing of the NCAM gene. We show that there is a distinct sequence of NCAM isoform expression during skeletal muscle development. Since NCAMs are also expressed in other cell types, particularly neurons, NCAM mRNAs have been colocalised with acetylcholine receptor alpha (AChR alpha) gene transcripts to identify muscle-specific expression. NCAM is first detected in somites as they first form, prior to their differentiation into muscle and nonmuscle compartments. Myotomes, the first skeletal muscle masses to form in the embryo, express mRNAs for the transmembrane 180 and 140 kDa isoforms of NCAM. Both of these transcripts are also detected in the neural tube, and their spatial pattern of expression changes with development. Transcripts containing the muscle-specific domain (MSD) of the NCAM gene are not detected prior to 11 days postcoitum (p.c.), at a time when rostral somites already contain well-developed myotomes. As the level of MSD mRNAs increases at 12 days p.c., the 140 and 180 kDa transcript levels decrease in skeletal muscle masses. The level of all NCAM isoform transcripts declines between 13 and 15 days p.c. in muscle. However, the 180 and 140 kDa NCAM isoforms are expressed at a high level in neural tissue and in other locations in the developing embryo such as in smooth muscle, around vibrissae follicles, and in the perichondrial zone of digits.

Animals↗
PubMed2005

The syntrophin-dystrobrevin subcomplex in human neuromuscular disorders.

The syntrophins and alpha-dystrobrevin form a subcomplex with dystrophin at the skeletal muscle membrane, and are also highly concentrated at the neuromuscular synapse. Here we demonstrate that the different syntrophins and alpha-dystrobrevin isoforms have distinct expression patterns during human skeletal muscle development, and are differentially affected by loss of dystrophin anchorage and denervation in human neuromuscular disease. During normal fetal development, and in Duchenne muscular dystrophy and denervation disorders, alpha1-syntrophin and alpha-dystrobrevin are absent or markedly reduced at the sarcolemmal membrane. beta1-Syntrophin is the predominant syntrophin isoform expressed at the muscle membrane during development, and it undergoes upregulation in response to loss of alpha1-syntrophin in Duchenne muscular dystrophy and in denervation. Upregulation of beta1-syntrophin in neuromuscular disorders is associated with re-expression of the fetal nicotinic acetylcholine receptor gamma-subunit, cardiac actin, and neonatal myosin, suggesting reversion of muscle fibers to an immature phenotype. We show that denervation specifically affects expression of the syntrophin-dystrobrevin subcomplex and does not affect levels or localization of other members of the dystrophin-associated protein complex. Our results confirm that dystrophin is required for anchorage of the syntrophin-dystrobrevin subcomplex and suggest that expression of the syntrophin-dystrobrevin complex may be independently regulated through neuromuscular transmission.

Animals↗
PubMed2005

Decreased isometric skeletal muscle force in critically ill patients.

QUESTION UNDER STUDY: Critically ill patients can develop muscle weakness that prolongs recovery. The aim of this study was to evaluate contractile parameters of the involuntary isometric skeletal muscle forces as measures of muscle weakness in critically ill patients. METHODS: Prospective, controlled trial performed in an intensive care unit (ICU) of a university hospital. SUBJECTS: 19 critically ill patients (diagnoses: intracranial bleeding n = 9; sepsis n = 6; others n = 4), who were ventilated and completely immobilised for one week. 20 healthy volunteers served as controls. We measured peak torques (PT), contraction times, half-relaxation times, peak rates of torque development and decay and torque latencies of the ankle dorsiflexors of the foot after peroneal nerve stimulation. RESULTS: Patients (median Acute Physiology and Chronic Health Evaluation II score 21) had reduced PTs, medians 3.3 Nm (interquartile range 2.5 Nm) vs 4.1 Nm (2.0 Nm) in controls (P = 0.0003) for single pulse, 4.9 (4.7) vs 8.1 Nm (3.8) (P = 0.0001) for 2-pulse, 6.1 (6.3) vs 10.3 Nm (3.9) (P = 0.0009) for 3-pulse and 7.3 (6.4) vs 11.6 Nm (7.8), (P = 0.006) for 4-pulse stimulations, respectively. Contraction times were reduced and half-relaxation times increased compared with controls. CONCLUSIONS: Assessment of involuntary isometric skeletal muscle forces can be readily measured in critically ill patients. After one week of critical illness, these patients have decreased force compared with healthy controls. This assessment approach will be further evaluated in a long-term study with a larger patient population.

APACHE↗
PubMed2005

The relationship between ciliary neurotrophic factor (CNTF) genotype and motor unit physiology: preliminary studies.

BACKGROUND: Ciliary neurotrophic factor (CNTF) is important for neuronal and muscle development, and genetic variation in the CNTF gene has been associated with muscle strength. The effect of CNTF on nerve development suggests that CNTF genotype may be associated with force production via its influence on motor unit size and firing patterns. The purpose of this study is to examine whether CNTF genotype differentially affects motor unit activation in the vastus medialis with increasing isometric force during knee extension. RESULTS: Sixty-nine healthy subjects were genotyped for the presence of the G and A (null) alleles in the CNTF gene (n = 57 G/G, 12 G/A). They were tested using a dynamometer during submaximal isometric knee extension contractions that were from 10-50% of their maximal strength. During the contractions, the vastus medialis was studied using surface and intramuscular electromyography with spiked triggered averaging to assess surface-detected motor unit potential (SMUP) area and mean firing rates (mFR) from identified motor units. CNTF genotyping was performed using standard PCR techniques from DNA obtained from leucocytes of whole blood samples. The CNTF G/A genotype was associated with smaller SMUP area motor units and lower mFR at higher force levels, and fewer but larger units at lower force levels than G/G homozygotes. The two groups used motor units with different size and activation characteristics with increasing force generation. While G/G subjects tended to utilize larger motor units with increasing force, G/A subjects showed relatively less increase in size by using relatively larger units at lower force levels. At higher force levels, G/A subjects were able to generate more force per motor unit size suggesting more efficient motor unit function with increasing muscle force. CONCLUSION: Differential motor unit responses were observed between CNTF genotypes at force levels utilized in daily activities.

Adult↗