Dysfunction of Neuromuscular Synaptic Transmission and Synaptic Vesicle Recycling in Motor Nerve Terminals of mSOD1 Transgenic Mice with Model of ... View Full Text


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Article Info

DATE

2019-01-03

AUTHORS

M. A. Mukhamedyarov, P. N. Grigoryev, G. A. Khisamieva, A. N. Khabibrakhmanov, E. A. Ushanova, A. L. Zefirov

ABSTRACT

Amyotrophic lateral sclerosis (ALS) is a progressive incurable neurodegenerative disease with selective loss of lower and upper motoneurons. Dysfunction and destruction of neuromuscular synapses leading to skeletal muscle denervation is one of the early and major events in ALS pathogenesis. Despite of the presence of studies devoted to investigation of neuromuscular transmission in ALS mouse models, no detailed information about molecular mechanisms underlying synaptic dysfunction in ALS and their temporal dynamics during ALS progression is provided. The goal of present work was to study the processes of neurotransmitter release and presynaptic vesicle recycling in neuromuscular synapses of mutated SOD1 (mSOD1) transgenic mice at different clinical stages of disease. Utilizing combination of electrophysiological recording and FM 1–43 (N-(3-triethylammoniumpropyl)-4-(4-(dibutylamino) styryl) pyridinium dibromide) fluorescent imaging, we found that mSOD1 mice at symptomatic and terminal stages of disease showed decreased baseline quantal content of end-plate potentials and prolonged synaptic vesicle recycling time comparing to wild-type mice. Despite the decrease of end-plate potential (EPP) quantal content, studied mSOD1 mice groups showed unchanged dynamics of EPP relative amplitude comparing to WT mice. We also found an increase of miniature end-plate potential amplitude in mSOD1 mice at symptomatic stage, which may reflect compensatory mechanism that alleviates reduction of EPP amplitude. Thus, we provided one of the first detailed characteristics of presynaptic dysfunction at neuromuscular junction in ALS model. Obtained data expand our understanding of the ALS pathogenesis and contribute to stage- and localization-specific description of ALS pathogenetic mechanisms. More... »

PAGES

66-73

References to SciGraph publications

  • 2009-04-24. Synaptic degeneration in Alzheimer’s disease in ACTA NEUROPATHOLOGICA
  • 2016-04-25. ALS: Recent Developments from Genetics Studies in CURRENT NEUROLOGY AND NEUROSCIENCE REPORTS
  • 2010-11-07. The “Dying-Back” Phenomenon of Motor Neurons in ALS in JOURNAL OF MOLECULAR NEUROSCIENCE
  • 2013-03-06. The changing scene of amyotrophic lateral sclerosis in NATURE REVIEWS NEUROSCIENCE
  • 2009-02-21. The vesicle cycle in motor nerve endings of the mouse diaphragm in NEUROSCIENCE AND BEHAVIORAL PHYSIOLOGY
  • 1993-03-01. Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis in NATURE
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    http://scigraph.springernature.com/pub.10.1007/s12668-018-0590-8

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    http://dx.doi.org/10.1007/s12668-018-0590-8

    DIMENSIONS

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