Specific impulse patterns regulate acetylcholinesterase activity in skeletal muscles of rats and rabbits

Sketelj, Janez; Leisner, Elmi; Gohlsch, Bärbel; Škorjanc, Dejan; Pette, Dirk

doi:10.1002/(sici)1097-4547(19970101)47:1<49::aid-jnr5>3.0.co;2-f

Cited by 29 publications

(4 citation statements)

References 44 publications

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“…104,105 Proteins characteristic of the synaptic specialization of fast-and slow-twitch muscles, such as acetylcholine esterase-1, are also affected. 161,162 Oxygen and fuel supply, and removal of metabolites and ions related to enhanced activity, are facilitated by an expansion of the extracellular space, 33,63 increased capillary density, 73,163 perfusion, 74 and myoglobin content. 80,176 Also, increases in satellite cell content have recently been demonstrated with low-frequency stimulation of rat muscle.…”

Section: Summary Of Changes Induced By Chronic Low-frequency Stimulationmentioning

confidence: 99%

What does chronic electrical stimulation teach us about muscle plasticity?

1999

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Section: Summary Of Changes Induced By Chronic Low-frequency Stimulationmentioning

confidence: 99%

What does chronic electrical stimulation teach us about muscle plasticity?

1999

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“…The expression of muscle functionality relies on the correct assembly of myofibrils, which comprise of tandem arrays of minimum contractile units, i.e., sarcomeres. Muscle activity such as excitation and contraction is known to regulate the expression and modification of a number of molecules such as acetylcholinesterase 4 , L-type Ca 2+ channels 5 , and glucose transporters 5 6 . Previously, it was reported that muscle fiber stimulation with electrical 7 8 9 , mechanical 10 11 , or pharmacological 12 13 methods, which mimic motor neuron inputs, facilitate the maturation of developing muscles as well as the maintenance of contractility.…”

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confidence: 99%

Optogenetic induction of contractile ability in immature C2C12 myotubes

Asano

Ishizuka

Morishima

et al. 2015

Sci Rep

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Myoblasts can be differentiated into multinucleated myotubes, which provide a well-established and reproducible muscle cell model for skeletal myogenesis in vitro. However, under conventional differentiation conditions, each myotube rarely exhibits robust contraction as well as sarcomere arrangement. Here, we applied trains of optical stimulation (OS) to C2C12 myotubes, which were genetically engineered to express a channelrhodopsin variant, channelrhodopsin-green receiver (ChRGR), to investigate whether membrane depolarization facilitates the maturation of myotubes. We found that light pulses induced membrane depolarization and evoked action potentials in ChRGR-expressing myotubes. Regular alignments of sarcomeric proteins were patterned periodically after OS training. In contrast, untrained control myotubes rarely exhibited the striated patterns. OS-trained and untrained myotubes also differed in terms of their resting potential. OS training significantly increased the number of contractile myotubes. Treatment with nifedipine during OS training significantly decreased the fraction of contractile myotubes, whereas tetrodotoxin was less effective. These results suggest that oscillations of membrane potential and intracellular Ca2+ accompanied by OS promoted sarcomere assembly and the development of contractility during the myogenic process. These results also suggest that optogenetic techniques could be used to manipulate the activity-dependent process during myogenic development.

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“…265 Fast NMJs, with larger synaptic depression from repetitive stimulation, 265 are specialised to resist this and ensure reliable transmission during prolonged stimulation through greater neurotransmitter release 265 and thus amplitude of the motor endplate potential, 263 increased density of acetylcholine receptors and voltage-dependent sodium channels in the postsynaptic folds, 266,267 and greater acetylcholinesterase activity that removes neurotransmitter of the NMJ. 268,269 Ageing has many adverse effects on NMJs, with consequences for sarcopenia and neurodegenerative diseases like ALS. 270 The changes during normal human age-related loss of muscle mass and function (i.e., sarcopenia) 7,271 correspond with changes during normal ageing of rodents.…”

Section: Nerves (And Vulnerability Of Fast Motoneurons)mentioning

confidence: 99%

“…Slow NMJs enable a sustained response to motoneurons during repetitive discharge through reduced synaptic depression (i.e., the reduction in neurotransmitter‐containing vesicles) compared with fast NMJs 265 . Fast NMJs, with larger synaptic depression from repetitive stimulation, 265 are specialised to resist this and ensure reliable transmission during prolonged stimulation through greater neurotransmitter release 265 and thus amplitude of the motor endplate potential, 263 increased density of acetylcholine receptors and voltage‐dependent sodium channels in the postsynaptic folds, 266,267 and greater acetylcholinesterase activity that removes neurotransmitter of the NMJ 268,269 . Ageing has many adverse effects on NMJs, with consequences for sarcopenia and neurodegenerative diseases like ALS 270 …”

Section: Myofibre‐type Differences Linked To Extrinsic Components Of ...mentioning

confidence: 99%

Slow or fast: Implications of myofibre type and associated differences for manifestation of neuromuscular disorders

et al. 2023

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Many neuromuscular disorders can have a differential impact on a specific myofibre type, forming the central premise of this review. The many different skeletal muscles in mammals contain a spectrum of slow‐ to fast‐twitch myofibres with varying levels of protein isoforms that determine their distinctive contractile, metabolic, and other properties. The variations in functional properties across the range of classic ‘slow’ to ‘fast’ myofibres are outlined, combined with exemplars of the predominantly slow‐twitch soleus and fast‐twitch extensor digitorum longus muscles, species comparisons, and techniques used to study these properties. Other intrinsic and extrinsic differences are discussed in the context of slow and fast myofibres. These include inherent susceptibility to damage, myonecrosis, and regeneration, plus extrinsic nerves, extracellular matrix, and vasculature, examined in the context of growth, ageing, metabolic syndrome, and sexual dimorphism. These many differences emphasise the importance of carefully considering the influence of myofibre‐type composition on manifestation of various neuromuscular disorders across the lifespan for both sexes. Equally, understanding the different responses of slow and fast myofibres due to intrinsic and extrinsic factors can provide deep insight into the precise molecular mechanisms that initiate and exacerbate various neuromuscular disorders. This focus on the influence of different myofibre types is of fundamental importance to enhance translation for clinical management and therapies for many skeletal muscle disorders.

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Specific impulse patterns regulate acetylcholinesterase activity in skeletal muscles of rats and rabbits

Cited by 29 publications

References 44 publications

What does chronic electrical stimulation teach us about muscle plasticity?

What does chronic electrical stimulation teach us about muscle plasticity?

Optogenetic induction of contractile ability in immature C2C12 myotubes

Slow or fast: Implications of myofibre type and associated differences for manifestation of neuromuscular disorders

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