Neural determination of muscle fibre numbers in embryonic rat lumbrical muscles

Development ◽  
1987 ◽  
Vol 100 (3) ◽  
pp. 395-409 ◽  
Author(s):  
J.J. Ross ◽  
M.J. Duxson ◽  
A.J. Harris
Keyword(s):  
Peripheral Nerves ◽  
Nerve Terminals ◽  
Normal Numbers ◽  
Myotube Formation ◽  
Physical Presence ◽  
Lumbrical Muscle ◽  
Lumbrical Muscles ◽  
Denervated Muscles ◽  
Intrinsic Muscles

The generation and development of muscle cells in the IVth hindlimb lumbrical muscle of the rat was studied following total or partial denervation. Denervation was carried out by injection of beta-bungarotoxin (beta-BTX), a neurotoxin which binds to and destroys peripheral nerves. Primary myotubes were generated in denervated muscles and reached their normal stable number on embryonic day 17 (E17). This number was not maintained and denervated muscles examined on E19 or E21 contained many degenerating primary myotubes. Embryos injected with beta-bungarotoxin (beta-BTX) on E12 or E13 suffered a partial loss of motoneurones, resulting in a reduced number of axons in the L4 ventral root (the IVth lumbrical muscle is supplied by axons in L4, L5 and L6 ventral roots) and reduced numbers of nerve terminals in the intrinsic muscles of the hindfoot. Twitch tension measurements showed that all myotubes in partly innervated muscles examined on E21 contracted in response to nerve stimulation. Primary myotubes were formed and maintained at normal numbers in muscles with innervation reduced throughout development, but a diminished number of secondary myotubes formed by E21. The latter was correlated with a reduction in number of mononucleate cells within the muscles. If beta-BTX was injected on E18 to denervate muscles after primary myotube formation was complete, E21 embryo muscles contained degenerating primary myotubes. After injection to denervate muscles on E19, the day secondary myotubes begin to form, E21 muscles possessed normal numbers of primary myotubes. In both cases, secondary myotube formation had stopped about 1 day after the injection and the number of mononucleate cells was greatly reduced, indicating that cessation of secondary myotube generation was most probably due to exhaustion of the supply of competent myoblasts. We conclude that nerve terminals regulate the number of secondary myotubes by stimulating mitosis in a nerve-dependent population of myoblasts and that activation of these myoblasts requires the physical presence of nerve terminals as well as activation of contraction in primary myotubes.

LIMB-GIRDLE MUSCULAR DYSTROPHY: ITS LARGER SIGNIFICANCE

PEDIATRICS ◽  
1968 ◽  
Vol 41 (2) ◽  
pp. 382-384
Author(s):  
S. C.
Keyword(s):  
Peripheral Nerves ◽  
Neuromuscular Disorders ◽  
Serum Enzymes ◽  
Muscle Disease ◽  
Muscular Dystrophies ◽  
Muscular Weakness ◽  
Conduction Velocities ◽  
Clinical Awareness ◽  
Muscle Biopsies

The current literature reflects the interest of pediatricians, neurologists, and internists in the neuromuscular disorders of childhood.1-5 Clinical awareness and the availability and refinement of ancillary procedures, such as electromyography, measurement of nerve conduction velocities, determination of serum enzymes and muscle biopsies, have made it possible to differentiate many of these conditions and correctly localize the pathology of these lower motor neuron disorders to the anterior horn cells, the peripheral nerves, and/or the muscles.1 Primary muscle disease is the most frequent cause of progressive muscular weakness in children with neuromuscular disorders.2 The primary myopathies are either hereditary or acquired. The muscular dystrophies and the myotonic syndrome are representative of the genetic variety, while the acquired disorders are recognized clinically as polymyositis and dermatomyositis.

Caffeine attenuates contraction-induced diminutions of the intracellular calcium transient in mouse lumbrical muscle ex vivo

2019 ◽  
Vol 97 (5) ◽  
pp. 429-435 ◽  
Author(s):  
Ian C. Smith ◽  
Rene Vandenboom ◽  
A. Russell Tupling
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Ex Vivo ◽  
Calcium Transient ◽  
Calcium Transients ◽  
Inotropic Effects ◽  
Intracellular Calcium Transient ◽  
Lumbrical Muscle ◽  
Lumbrical Muscles

The amount of calcium released from the sarcoplasmic reticulum in skeletal muscle rapidly declines during repeated twitch contractions. In this study, we test the hypothesis that caffeine can mitigate these contraction-induced declines in calcium release. Lumbrical muscles were isolated from male C57BL/6 mice and loaded with the calcium-sensitive indicator, AM-furaptra. Muscles were then stimulated at 8 Hz for 2.0 s in the presence or absence of 0.5 mM caffeine, at either 30 °C or 37 °C. The amplitude and area of the furaptra-based intracellular calcium transients and force produced during twitch contractions were calculated. For each of these measures, the values for twitch 16 relative to twitch 1 were higher in the presence of caffeine than in the absence of caffeine at both temperatures. We conclude that caffeine can attenuate contraction-induced diminutions of calcium release during repeated twitch contractions, thereby contributing to the inotropic effects of caffeine.

Laser ablation of persistent twist cells in Drosophila: muscle precursor fate is not segmentally restricted

Development ◽  
1999 ◽  
Vol 126 (2) ◽  
pp. 273-280 ◽  
Author(s):  
E.R. Farrell ◽  
H. Keshishian
Keyword(s):  
Transcription Factor ◽  
Laser Ablation ◽  
Muscle Fiber ◽  
Peripheral Nerves ◽  
Abdominal Segment ◽  
Muscle Fibers ◽  
Normal Numbers ◽  
Developmental Potential ◽  
Lateral Muscle ◽  
Adjacent Segments

In Drosophila the precursors of the adult musculature arise during embryogenesis. These precursor cells have been termed Persistent Twist Cells (PTCs), as they continue to express the transcription factor Twist after that gene ceases expression elsewhere in the mesoderm. In the larval abdomen, the PTCs are associated with peripheral nerves in stereotypic ventral, dorsal, and lateral clusters, which give rise, respectively, to the ventral, dorsal, and lateral muscle fiber groups of the adult. We tested the developmental potential of the PTCs by using a microbeam laser to ablate specific clusters in larvae. We found that the ablation of a single segmental PTC cluster does not usually result in the deletion of the corresponding adult fibers of that segment. Instead, normal or near normal numbers of adult fibers can form after the ablation. Examination of pupae following ablation showed that migrating PTCs from adjacent segments are able to invade the affected segment, replenishing the ablated cells. However, the ablation of homologous PTCs in multiple segments does result in the deletion of the corresponding adult muscle fibers. These data indicate that the PTCs in an abdominal segment can contribute to the formation of muscle fibers in adjacent abdominal segments, and thus are not inherently restricted to the formation of muscle fibers within their segment of origin.

scholarly journals Brain dynein (MAP1C) localizes on both anterogradely and retrogradely transported membranous organelles in vivo.

1990 ◽  
Vol 111 (3) ◽  
pp. 1027-1037 ◽  
Author(s):  
N Hirokawa ◽  
R Sato-Yoshitake ◽  
T Yoshida ◽  
T Kawashima
Keyword(s):  
Nerve Terminal ◽  
Peripheral Nerves ◽  
Molecular Motor ◽  
Retrograde Transport ◽  
Nerve Terminals ◽  
Electron Microscopic ◽  
Electron Microscopic Immunocytochemistry ◽  
Fast Flow

Brain dynein is a microtubule-activated ATPase considered to be a candidate to function as a molecular motor to transport membranous organelles retrogradely in the axon. To determine whether brain dynein really binds to retrogradely transported organelles in vivo and how it is transported to the nerve terminals, we studied the localization of brain dynein in axons after the ligation of peripheral nerves by light and electron microscopic immunocytochemistry using affinity-purified anti-brain dynein antibodies. Different classes of organelles preferentially accumulated at the regions proximal and distal to the ligated part. Interestingly, brain dynein accumulated both at the regions proximal and distal to the ligation sites and localized not only on retrogradely transported membranous organelles but also on anterogradely transported ones. This is the first evidence to show that brain dynein associates with retrogradely transported organelles in vivo and that brain dynein is transported to the nerve terminal by fast flow. This also suggests that there may be some mechanism that activates brain dynein only for retrograde transport.

An analysis of acetylcholine in frog muscle by mass fragmentography

1977 ◽  
Vol 197 (1128) ◽  
pp. 285-297 ◽  
Keyword(s):  
Synaptic Vesicles ◽  
Motor Nerve ◽  
Gas Chromatography Mass Spectrometry ◽  
Sartorius Muscle ◽  
Nerve Terminals ◽  
Mass Fragmentography ◽  
Pyrolysis Gas ◽  
Free Region ◽  
Denervated Muscles ◽  
Frog Sartorius

Extracts of frog sartorius muscles were assayed for their acetylcholine (ACh) content by means of pyrolysis-gas chromatography/mass spectrometry. Freshly dissected whole muscles contained 43 ± 3.1 (22) pmol ACh, and apart from ACh, no other related ester was detected. The ACh content varied among different animals, but was relatively independent of muscle mass. In denervated muscles the ACh content began to decrease after a delay of two days and, by the eighth day of denervation, reached a steady value of about 26% of the control. Muscles were divided into endplate free segments and segments containing endplates. ACh was localized predominantly in the endplate segment, but a small amount was found in the endplate free region. The endplate segments of denervated muscles contained ACh at the same low concentration as ACh in non-endplate segments. The ACh concentration in non-endplate segments was not affected by denervation. During incubation in the presence of diisopropylfluorophosphate muscles released 2.1 pmol/h into the medium. During the incubation the ACh content of the muscles remained constant. It is concluded that there is about 12 pmol extraneural ACh in sartorius muscle, and that about 30 pmol is in the nerve terminals. If it is assumed that one half of the neural ACh is contained in the synaptic vesicles of motor nerve terminals, then each vesicle would contain, on the average, some 8 x 10 3 molecules of ACh.

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