scholarly journals ROLE of exercise in maintaining the integrity of the neuromuscular junction

2013 ◽  
Vol 49 (3) ◽  
pp. 315-324 ◽  
Author(s):  
Hiroshi Nishimune ◽  
John A. Stanford ◽  
Yasuo Mori
Keyword(s):  
Neuromuscular Junction

The Significance of Brain Acetylcholine

1953 ◽  
Vol 99 (415) ◽  
pp. 247-251 ◽  
Author(s):  
J. Crossland
Keyword(s):  
Neuromuscular Junction ◽  
Synaptic Transmission ◽  
Nervous Transmission ◽  
Central Synapses ◽  
Brain Acetylcholine ◽  
Fundamental Action ◽  
Synaptic Transmitter

Until a few years ago there existed a sharp dichotomy of opinion between the pharmacologists, who, on the basis of their experiments, assigned to acetylcholine the role of universal synaptic transmitter, and the electrophysiologists, who denied that this substance could effect the transfer of excitation from one conducting element to another. It is, however, now generally agreed that, certainly at the neuromuscular junction, and probably also at ganglionic and some—but not all—central synapses, acetylcholine does indeed exert a primary transmitter action. It must be added that recognition of this fundamental action has been hastened as a result of recent experiments by those very electrophysiologists (such as Eccles and his colleagues) who previously supported exclusively electrical hypotheses of nervous transmission. For this reason the assumption which is implicit throughout this paper that the acetylcholine in brain is concerned in maintaining central synaptic transmission is likely to go unchallenged and requires no detailed justification here.

scholarly journals Role of intracellular Ca2+ in stimulation-induced increases in transmitter release at the frog neuromuscular junction.

1994 ◽  
Vol 104 (2) ◽  
pp. 337-355 ◽  
Author(s):  
J E Zengel ◽  
M A Sosa ◽  
R E Poage ◽  
D R Mosier
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Cyclopiazonic Acid ◽  
Progressive Increase ◽  
Repetitive Stimulation ◽  
Frog Neuromuscular Junction ◽  
Quantal Content ◽  
Carbonyl Cyanide ◽  
Stimulation Of

Under conditions of reduced quantal content, repetitive stimulation of a presynaptic nerve can result in a progressive increase in the amount of transmitter released by that nerve in response to stimulation. At the frog neuromuscular junction, this increase in release has been attributed to four different processes: first and second components of facilitation, augmentation, and potentiation (e.g., Zengel, J. E., and K. L. Magleby. 1982. Journal of General Physiology. 80:583-611). It has been suggested that an increased entry of Ca2+ or an accumulation of intraterminal Ca2+ may be responsible for one or more of these processes. To test this hypothesis, we have examined the role of intracellular Ca2+ in mediating changes in end-plate potential (EPP) amplitude during and after repetitive stimulation at the frog neuromuscular junction. We found that increasing the extracellular Ca2+ concentration or exposing the preparation to carbonyl cyanide m-chlorophenylhydrazone, ionomycin, or cyclopiazonic acid all led to a greater increase in EPP amplitude during conditioning trains of 10-200 impulses applied at a frequency of 20 impulses/s. These experimental manipulations, all of which have been shown to increase intracellular levels of Ca2+, appeared to act by increasing primarily the augmentation component of increased release. The results of this study are consistent with previous suggestions that the different components of increased release represent different mechanisms, and that Ca2+ may be acting at more than one site in the nerve terminal.

Emerging role of neuregulin as a modulator of muscle metabolism

2010 ◽  
Vol 298 (4) ◽  
pp. E742-E750 ◽  
Author(s):  
Anna Gumà ◽  
Vicente Martínez-Redondo ◽  
Iliana López-Soldado ◽  
Carles Cantó ◽  
Antonio Zorzano
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Neuromuscular Junction ◽  
Muscle Contraction ◽  
Neurotrophic Factor ◽  
Muscle Metabolism ◽  
Metabolic Effects ◽  
Energetic Metabolism ◽  
Insulin Responsiveness

Neuregulin was described initially as a neurotrophic factor involved in the formation of the neuromuscular junction in skeletal muscle. However, in recent years, neuregulin has been reported to be a myokine that exerts relevant effects on myogenesis and the regulation of muscle metabolism. In this new context, the rapid and chronic metabolic effects of neuregulin appear to be related to muscle contraction. Indeed, the effects of neuregulin resemble those of exercise, which are accompanied by an improvement in insulin sensitivity. In this review, we challenge the classical role assigned to neuregulin in muscle and propound the emerging concept of its involvement in the regulation of energetic metabolism and insulin responsiveness.

scholarly journals FOXO regulates neuromuscular junction homeostasis during Drosophila aging

2020 ◽  
Author(s):  
Allison Birnbaum ◽  
Kai Chang ◽  
Hua Bai
Keyword(s):  
Neuromuscular Junction ◽  
Motor Neuron ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Late Endosomes ◽  
Age Dependent ◽  
Neuronal Processes ◽  
Longitudinal Muscles ◽  
Adult Drosophila

AbstractThe transcription factor FOXO is a known regulator of lifespan extension and tissue homeostasis. It has been linked to the maintenance of neuronal processes across many species, and has been shown to promote youthful characteristics by regulating cytoskeletal flexibility and synaptic plasticity at the neuromuscular junction (NMJ). However, the role of FOXO in aging neuromuscular junction function has yet to be determined. We profiled adult Drosophila FOXO-null mutant abdominal ventral longitudinal muscles and found that young mutants exhibited morphological profiles similar to those of aged wild-type flies, such as larger bouton areas and shorter terminal branches. We also observed changes to the axonal cytoskeleton and an accumulation of late endosomes in FOXO null mutants and motor neuron-specific FOXO knockdown flies, similar to those of aged wild-types. Motor neuron-specific overexpression of FOXO can delay age-dependent changes to NMJ morphology, suggesting FOXO is responsible for maintaining NMJ integrity during aging. Through genetic screening, we identify several downstream factors mediated through FOXO-regulated NMJ homeostasis, including genes involved in the p38-MAPK pathway. Interestingly, the phosphorylation of p38 and ERK were increased in the motor neuron-specific FOXO knockdown flies, suggesting FOXO acts as a suppressor of MAPK activation. Our work reveals that FOXO is a key regulator for NMJ homeostasis, and it maintains NMJ integrity by repressing MAPK signaling during aging.

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