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At least 289 records · Page 16Linked to original sources
PubMed1984

Possible migration of imaginal myoblasts from adjacent nerve sheath into the developing flight muscle of Chironomus.

The emplacement of the first imaginal myoblasts along the larval muscles which are precursors of the dorsal longitudinal flight muscles, has been studied in Chironomus (Diptera, Nematocera), by light and electron microscopy. At the beginning of larval life there are no imaginal myoblasts stored along these muscles. These cells are discerned only at the beginning of the last larval instar. They first appear in the median region of the muscles near the neuromuscular junction. Prior to this, however, there are cells possessing the same cytological characteristics as the imaginal myoblasts inside the sheath of the motor nerves that supply the muscles. These observations suggest that myoblasts could arrive by the nerve sheath. The presence of a thick, continuous basal lamina around the larval muscles seems to exclude all other possibility of access to these muscles. The extension of this hypothesis to the Cyclorrhaphan Diptera is discussed.

Animals↗
PubMed1981

Different actions of calcium channel blocking agents on resting membrane conductance in developing skeletal muscle.

The effects of Co2+, Mn2+, and La3+ (2 mM) and verapamil (5 x 10(-6) M) on membrane conductance (Gm) and resting potential (Em) were studied in chick skeletal muscle fibres developing in culture. Cobalt and manganese had no effect on Gm at any time during myogenesis but verapamil caused a decrease in Gm in immature myotubes. This effect diminished with time and was absent by 3 days after myoblast fusion. Lanthanum caused an increase in Gm at all stages of development. All the agents studied caused a significant depolarization of Em. It is concluded that there is no resting calcium conductance in developing skeletal muscle but that there may be a resting sodium conductance which declines with maturation. Lanthanum may increase Gm by displacing membrane-bound calcium and destabilizing membrane structure. All the agents studied were thought to induce depolarization by an inhibitory action on (Na+ + K+)-ATPase.

Animals↗
PubMed1995

Modulation of a potassium conductance in developing skeletal muscle.

K+ conductances dominate and potentially modulate the resting potential of skeletal muscle cells. The expression and modulation of a major K+ conductance were examined during in vitro differentiation of the mouse myoblast cell line C2C12. The inwardly rectifying K+ conductance (IKi) increased from unmeasurable levels in undifferentiated myoblasts to approximately 1.56 +/- 0.51 nA (n = 17) in myoballs derived from myotubes at 5 days after induction of differentiation. The inward rectifier was subject to modulation by intracellular signals. Exposure of cytoplasm to guanosine 5'-O-(3-thiotriphosphate) during whole cell recording produced a concentration (5-100 microM)- and time (1-20 min)-dependent inhibition of the mean conductance. Elevation of intracellular free Ca2+ (> 200 nM) also inhibited IKi. These findings demonstrate a potential mechanism for modulation of the resting potential of muscle fibers via the control of skeletal muscle IKi.

Animals↗
PubMed1988

[Calpains, protein kinase c and development of muscle tissue].

Calpains are Ca2+ -dependent thiol proteases which have been identified in various tissues of eucaryotes, but their physiological function in the cell is uncertain. In the muscle fiber, two types of calpains are present which differ by their calcium sensitivity: calpain 1 and calpain 2, which require for their activity micro and millimolar concentrations of calcium respectively. These calpains are associated with protein kinase C activities in the differentiated fiber. The multinucleate myotube is formed by fusion of mononucleated precursor cells, myoblasts. Calpains have been reported to appear in myoblasts at around the time of fusion. Moreover, an apparent synthesis of 1,2 diacylglycerol, an activator of protein kinase C, was observed during fusion of myoblasts. However, more information is required to incriminate totally protein kinase C and calpains in the mechanism of myoblast fusion.

Animals↗
PubMed1987

Adult forms of the Ca2+ATPase of sarcoplasmic reticulum. Expression in developing skeletal muscle.

Two separate genes encode fast-twitch and slow-twitch/cardiac muscle forms of the Ca2+ ATPase of sarcoplasmic reticulum. Full length Ca2+ ATPase clones have been isolated from adult rabbit fast-twitch, slow-twitch, and cardiac muscles. Segments of these clones containing unique sequences have been used as probes to study developmental changes in Ca2+ ATPase transcripts. The fast-twitch Ca2+ ATPase transcript undergoes developmentally regulated alternative splicing in which a penultimate 42-base pair exon is retained in the adult transcript but is excised in the neonatal transcript. This additional exon shifts the exon encoding the neonatal carboxyl-terminal sequence, -Asp-Pro-Glu-Asp-Glu-Arg-Arg-Lys (Brandl, C. J., Green, N. M., Korczak, B., and MacLennan, D. H. (1986) Cell 44, 597-607) into a nontranslated region and results in the expression of an adult isoform with a carboxyl-terminal -Gly. The neonatal form of the fast-twitch Ca2+ ATPase represents 72% of the fast-twitch Ca2+ ATPase transcripts just prior to birth but only 17% by 14 days of age and 4% in adult fast-twitch muscle. Adult slow-twitch, adult cardiac, and neonatal skeletal muscles express an identical Ca2+ATPase mRNA transcript which is distinct from either of the fast-twitch forms. The slow-twitch/cardiac Ca2+ ATPase is the predominant form expressed in late fetal and early neonatal rabbit skeletal muscle, but this form is lost as the skeletal muscle differentiates into a fast-twitch state. Three or more alternative polyadenylation signals exist for this mRNA in all tissues with the most 3' signal predominating.

Aging↗