Physiological properties of nerve-muscle junctions developing in vivo.
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Acetylcholine↗
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Tetrodotoxin-sensitive sodium channels in rat muscle cells developing in vitro.
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Animals↗
Effects of thyroid hormone on mRNAs of phosphoglycerate mutase subunits in rat muscle during development.
BACKGROUND: We previously showed that triiodothyronine (T3) stimulates muscle phosphoglycerate mutase (PGAM) activity and isozyme transition in rat skeletal and cardiac muscles. METHODS: The effects of T3 on PGAM types B and M subunit expression in rat muscle during development are reported. RESULTS: T3 administration during the first 21 days of rat life more than doubles type M PGAM mRNA levels, but produces minor effects on type B PGAM mRNA levels. The antihormone propylthiouracil (PTU) slightly decreases both type B and M mRNA levels, but this decrease is not statistically significant. CONCLUSION: Thyroid hormone influences PGAM mRNA isozyme levels differently and increases type M mRNA.
Animals↗
Insulin-like growth factor-II expression in developing skeletal muscle of double muscled and normal cattle.
Double muscled (DM) cattle possess nearly 40% more muscle fibers than normal muscled (NM) beef or dairy cattle. Previous work showed that serum from DM fetuses stimulated proliferation of L6 myoblasts to a greater extent than serum from NM fetuses. Although the exact role of insulin-like growth factor-II (IGF-II) in the regulation of fetal myogenesis is unknown, it has been shown to serve as a autocrine-acting growth factor during terminal differentiation of myoblasts in mitogen-depleted culture media. Delay of IGF-II expression may alter the ultimate number of muscle fibers formed during fetal development. To investigate this, forty-seven skeletal muscle and twenty-nine liver samples were collected from NM fetuses representing fetuses grouped by crown-rump lengths (CRL) of < 20, 21-30, 31-40, 41-50, 51-60, 61-70 or > 70 cm. Twelve DM fetuses representing 20, 40, 50, and 85 cm were compared to NM groups with the same CRL. Total RNA preparations from these samples were subjected to northern and dot blot analysis using rat IGF-II and beta actin cDNAs and a human 28S rRNA oligomer. IGF-II transcripts of 4.5, 3.6, 2.75, 2.5, and 1.15 kilobases (kb) were detected in liver and muscle RNA from both DM and NM fetuses. Liver IGF-II expression increased (P < 0.05) in both DM and NM fetuses with CRL. Mean concentrations of muscle IGF-II mRNA initially increased (P < 0.05), then decreased (P < 0.05) with CRL in DM and NM fetuses. Muscle IGF-II mRNA was greater (P < 0.05) for NM fetuses compared to DM fetuses at 20 cm CRL, whereas at 53 cm CRL, DM muscle IGF-II was greater (P < 0.05) than that of NM fetuses. These results show that the maximum expression of muscle IGF-II is delayed in DM fetuses compared to NM fetuses. This delayed expression may play an explicit role in controlling myogenesis in the development of double muscle cattle.
Analysis of Variance↗
Training-induced changes in muscle CSA, muscle strength, EMG, and rate of force development in elderly subjects after long-term unilateral disuse.
The ability to develop muscle force rapidly may be a very important factor to prevent a fall and to perform other tasks of daily life. However, information is still lacking on the range of training-induced neuromuscular adaptations in elderly humans recovering from a period of disuse. Therefore, the present study examined the effect of three types of training regimes after unilateral prolonged disuse and subsequent hip-replacement surgery on maximal muscle strength, rapid muscle force [rate of force development (RFD)], muscle activation, and muscle size. Thirty-six subjects (60-86 yr) were randomized to a 12-wk rehabilitation program consisting of either 1) strength training (3 times/wk for 12 wk), 2) electrical muscle stimulation (1 h/day for 12 wk), or 3) standard rehabilitation (1 h/day for 12 wk). The nonoperated side did not receive any intervention and thereby served as a within-subject control. Thirty subjects completed the trial. In the strength-training group, significant increases were observed in maximal isometric muscle strength (24%, P < 0.01), contractile RFD (26-45%, P < 0.05), and contractile impulse (27-32%, P < 0.05). No significant changes were seen in the two other training groups or in the nontrained legs of all three groups. Mean electromyogram signal amplitude of vastus lateralis was larger in the strength-training than in the standard-rehabilitation group at 5 and 12 wk (P < 0.05). In contrast to traditional physiotherapy and electrical stimulation, strength training increased muscle mass, maximal isometric strength, RFD, and muscle activation in elderly men and women recovering from long-term muscle disuse and subsequent hip surgery. The improvement in both muscle mass and neural function is likely to have important functional implications for elderly individuals.
Aged↗
Development of the anal canal muscles.
The anal canal muscles development is studied in 18 human embryos. The external anal sphincter results to origin common with the urogenital sphincter from the cloacal sphincter. The muscle, after its appearance, is subdivided into two portions from a thin mesenchymal layer. Moreover, our embryologic study clearly confirms that the puborectalis muscle is a portion of the levator ani, its primordium being common with the ileo and the pubococcygeus muscles. The anal smooth musculature appears later than the striated one.
Anal Canal↗
Patterns of amino acid enzyme in domestic fowl breast and leg muscle during development.
Activities of alanine and aspartate transaminases, glutamine synthetase, adenylate deaminase, glutamate and xanthine dehydrogenases and lactate dehydrogenase were measured in leg and breast muscles of developing chicks from day 10 in ovo to day 5 of free life, and compared with measurements for adult hens. Xanthine dehydrogenase activity was low in both muscles with adult levels attained on day 15 in ovo. Glutamine synthetase for chicks was maintained higher during development than for adults in both muscles. Minor differences were observed between both muscles in all enzymes tested up to day 18. With low embryonic values and important rises before hatching, the differences were initiated in the posthatching period. Important differences were observed between adult levels of activity. Leg muscle revealed higher enzyme values except for lactate dehydrogenase and indistinguishable levels for adenylate deaminase and xanthine dehydrogenase in both muscles. Alanine, instead of glutamine, is postulated as the main nitrogen transport between muscle and liver in the domestic fowl.
AMP Deaminase↗
Effects of hypothyroidism on myosin isozyme transitions in developing rat muscle.
Hypothyroidism was induced in young rats by methylthiouracil treatment of pregnant mothers from 18 days of gestation to 4 weeks after birth. Electrophoretic analysis of native myosin isozymes revealed a persistence of neonatal and embryonic myosin in developing fast and slow muscles up to at least 28 days after birth. The appearance of adult fast myosin was inhibited in 28-day old animals, however adult slow myosin was found in the soleus muscle. Immunocytochemical results on the soleus demonstrate a cellular heterogeneity in the response to hypothyroidism. About half fibers have a normal complement of slow myosin and do not contain neonatal myosin. Only the remaining fibers contain the large amounts of neonatal myosin demonstrated by electrophoresis.
Age Factors↗
Chloride channels of skeletal muscle from developing, adult and aged rats are differently affected by enantiomers of 2-(p-chlorophenoxy) propionic acid.
Enantiomers of 2-(p-chlorophenoxy) propionic acid, compounds acting specifically on chloride channels of adult rat skeletal muscles, have been tested on extensor digitorum longus (EDL) muscle of developing and aged rats, in an attempt to characterize the chloride channels responsible for the low chloride conductance (GCl) found in the above physiological situations. The S-(-) enantiomer, which produces a concentration-dependent inhibition of GCl in the adult EDL, is less effective in inhibiting GCl of EDL of either 2-3 weeks or 29 months old rats, particularly at low concentrations. The R-(+) isomer, which in the adult enhances GCl at low concentrations and blocks it at concentrations higher than 10 microM, lacks inhibitory action, enhancing GCl in both developing and aged EDL. At 30-40 days of age both the enantiomers produce almost the same effects exerted in adulthood. From these data we hypothesize that the low GCl found in EDL of developing and aged rats might be due not only to a lower number of conductive channels but also to the presence of a mixed population of isoforms of chloride channels having different pharmacological properties.
2-Methyl-4-chlorophenoxyacetic Acid↗
Mechanism of neuronal coordination of the rhythmic activities of developing flight muscles and a neurosecretory cell population in the silkmoth, Bombyx mori.
Ultradian rhythmic firing activity (period of 40-90 min) of a population of neurosecretory cells (NSCs) producing FXPRLamide peptides in the subesophageal ganglion (SG) of the silkmoth, Bombyx mori, is closely coordinated with periodically occurring electrical activity of developing flight muscles (FMs) during metamorphosis. To examine neuronal mechanisms and pathways that mediate the coordination of the NSC and flight motor systems, the ventral nerve cord (VNC) or circumesophageal connectives were transected. Transection of the VNC between the SG and thoracic ganglia greatly shortened the period of activity rhythm of the FMs (5-15 min) with no effect on the rhythmicity of NSCs. Bilateral transsection of the circumesophageal connectives between the brain and SG abolished the rhythmic activity of NSCs, thereby suggesting that the coordination of the two systems may be mediated by a common oscillatory mechanism in the brain. Further, bisection of the brain in the midline failed to abolish the ultradian rhythmicity of FMs. Thus, each brain hemisphere may have an ultradian oscillator that activates the NSC system in the SG, and modulates the short-period oscillation of the flight motor system located in the thoracic ganglia.
Action Potentials↗
The capacity of the sarcoplasmic reticulum for phospholipid synthesis: a developmental study.
The activities of three enzymes involved in phospholipid synthesis, sn-glycerol-3-phosphate acyltransferase (EC 2.3.1.15), cholinephosphate cytidylyltransferase (EC 2.7.7.15), and cholinephosphotransferase (EC 2.7.8.2), were assayed in adult skeletal muscle. The acyltransferase and cholinephosphotransferase were concentrated in the sarcoplasmic reticulum, where their specific activities were 80 and 33%, respectively, of the specific activity in liver microsomes. Cytidylyltransferase activity was distributed throughout the cell with most of the activity in the cytosol. Its activity in muscle was only 10% of liver activity. Functional sarcoplasmic reticulum was isolated by density gradient centrifugation after calcium loading in the presence of phosphate. The specific activities of these enzymes wee undiminished in the calcium-loaded fraction, suggesting that these enzymes are intrinsic components of the sarcoplasmic reticulum. In developing muscle (2 and 6 days postnatal) acyltransferase and cholinephosphotransferase activities were also present in a calcium-loaded microsomal subfraction at the same level as in the adult. Cytidylyltransferase activity, on the other hand, was 8-fold higher in developing muscle. In addition, developing muscle had a 3-fold increase in the proportion of cytidylyltransferase associated with the microsomal fraction. These data suggest that sarcoplasmic reticulum has the capacity for phospholipid synthesis in mature and developing muscle, and that the rate of phosphatidylcholine synthesis may be regulated by the levels of cytidylyltransferase and by translocation of this enzyme between the sarcoplasmic reticulum and the cytosol.
Animals↗
Calcium accumulation by isolated sarcoplasmic reticulum of skeletal muscle during development in tissue culture.
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Adenosine Triphosphatases↗
[Aspects of prenatal development of muscle and adipose tissue: principles, regulation, and influence of maternal nutrition].
During pregnancy the developing embryo/foetus is completely dependent on the supply with nutrients and the removal of metabolic by-products through the maternal organism. Therefore, each lasting inadequate nutrient supply may have serious consequences for foetal development. As a kind of "nutritional programming" resulting adaptive changes may be maintained until or manifested at adult age. Intrauterine growth retardation (IUGR) may cause problems in animal health and result in poor animal performance. The relationships between prenatal development and the postnatal phenotypic appearance of muscle and fat are insufficiently investigated. The present paper provides selected aspects of the prenatal development of skeletal muscle (myogenesis) and adipose tissue (adipogenesis), refers to the importance of interactions between both tissues and is focussed on the influence of maternal nutrition on these processes.
Adipogenesis↗
Proliferation and differentiation of human fetal myoblasts is regulated by PDGF-BB.
A myoblast clone, G6, was obtained from thigh muscle of an 11 week old human fetus, and used to examine the effect of platelet-derived growth factor (PDGF) on cell multiplication and differentiation. G6 myoblasts showed extensive fusion, and expressed creatine phosphokinase activity and muscle specific gene mRNA (myosin heavy chain, alpha-actin) when switched to a differentiation medium. The cells expressed PDGF beta-receptor mRNA, and bound 125I-PDGF-BB specifically. Expression of PDGF beta-receptors declined during in vitro differentiation. Relative levels of transcripts for the myogenic regulatory factors Myf4 (myogenin), Myf5, and Myf6 (MRF4) increased during the differentiation process, whereas Myf3 (MyoD1) was preferentially expressed in undifferentiated myoblasts. Treatment of the myoblasts with PDGF-BB increased DNA synthesis and cell density. Myogenic differentiation, analyzed as number of nuclei present in myotubes and expression of creatine phosphokinase and myosin heavy chain, was partly inhibited by the presence of PDGF-BB in the differentiation medium. PDGF-BB may, therefore, have the potential of regulating human muscle development and muscle regeneration.
Becaplermin↗
Overlapping functions of the myogenic bHLH genes MRF4 and MyoD revealed in double mutant mice.
The myogenic basic helix-loop-helix (bHLH) genes - MyoD, Myf5, myogenin and MRF4 - exhibit distinct, but overlapping expression patterns during development of the skeletal muscle lineage and loss-of-function mutations in these genes result in different effects on muscle development. MyoD and Myf5 have been shown to act early in the myogenic lineage to establish myoblast identity, whereas myogenin acts later to control myoblast differentiation. In mice lacking myogenin, there is a severe deficiency of skeletal muscle, but some residual muscle fibers are present in mutant mice at birth. Mice lacking MRF4 are viable and have skeletal muscle, but they upregulate myogenin expression, which could potentially compensate for the absence of MRF4. Previous studies in which Myf5 and MRF4 null mutations were combined suggested that these genes do not share overlapping myogenic functions in vivo. To determine whether the functions of MRF4 might overlap with those of myogenin or MyoD, we generated double mutant mice lacking MRF4 and either myogenin or MyoD. MRF4/myogenin double mutant mice contained a comparable number of residual muscle fibers to mice lacking myogenin alone and myoblasts from those double mutant mice formed differentiated multinucleated myotubes in vitro as efficiently as wild-type myoblasts, indicating that neither myogenin nor MRF4 is absolutely essential for myoblast differentiation. Whereas mice lacking either MRF4 or MyoD were viable and did not show defects in muscle development, MRF4/MyoD double mutants displayed a severe muscle deficiency similar to that in myogenin mutants. Myogenin was expressed in MRF4/MyoD double mutants, indicating that myogenin is insufficient to support normal myogenesis in vivo. These results reveal unanticipated compensatory roles for MRF4 and MyoD in the muscle differentiation pathway and suggest that a threshold level of myogenic bHLH factors is required to activate muscle structural genes, with this level normally being achieved by combinations of multiple myogenic bHLH factors.
Animals↗
The effects of deafferentation and spinal cord transection on synapse elimination in developing rat muscles.
The proportion of muscle fibres innervated by more than one motoneurone (polyneuronal innervation) was measured in the fourth deep lumbrical muscle of young rats following either unilateral deafferentation or spinal cord isolation (cord transection combined with bilateral deafferentation). 2. Unilateral deafferentation at 7 days of age did not affect the subsequent time course of synapse elimination in the developing muscle. 3. Spinal cord isolation at 7 days led to a prolongation of the time course of synapse elimination in the muscle, levels of polyneuronal innervation approaching zero beyond about 30 days (about 20 days in normal animals). The raised levels of polyneuronal innervation in these animals were not associated with significant terminal sprouting at end-plates, but were associated with multiple axonal inputs to end-plates as is found in younger normal animals. This was shown by zinc iodide and osmium staining. Also some muscle fibres had two and sometimes three separate end-plates. 4. Spinal cord isolation in rats 19 or more days old resulted in a reappearance of multiple innervation. This was largely due to ultraterminal sprouting. 5. It is concluded that unilateral deafferentation alone causes no change in the time course of synapse elimination. The multiple innervation caused by total deafferentation and spinal transection is attributed to the lack of activity of these muscles.
Aging↗
The relation between blood flow and enzymatic activities in slow and fast muscles during development.
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Age Factors↗
Localization of VEGF-B in the mouse embryo suggests a paracrine role of the growth factor in the developing vasculature.
Vascular endothelial growth factor B (VEGF-B) is structurally closely related to VEGF and binds one of its receptors, VEGFR-1. In situ hybridization and immunohistochemistry were used to localize VEGF-B mRNA and protein in embryonic mouse tissues. In 8.5-17.5 day embryos, VEGF-B was most prominently expressed in the developing myocardium, but not in the cardiac cushion tissue. The strong expression in the heart persisted at later developmental stages, while weaker signals were obtained from several other tissues, including developing muscle, bone, pancreas, adrenal gland, and from the smooth muscle cell layer of several larger vessels, but not from endothelial cells. VEGF-B is likely to act in a paracrine fashion, as its receptor is almost exclusively present in endothelial cells. VEGF-B may have a role in vascularization of the heart, skeletal muscles and developing bones, and in paracrine interactions between endothelial and surrounding muscle cells.
Animals↗