Казанский (Приволжский) федеральный университет, КФУ
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HOMOCYSTEINE AGGRAVATES ROS-INDUCED DEPRESSION OF TRANSMITTER RELEASE FROM MOTOR NERVE TERMINALS: POTENTIAL MECHANISM OF PERIPHERAL IMPAIRMENT IN MOTOR NEURON DISEASES ASSOCIATED WITH HYPERHOMOCYSTEINEMIA
Форма представленияСтатьи в зарубежных журналах и сборниках
Год публикации2015
Языкрусский
  • Бухараева Элля Ахметовна, автор
  • Гиниатуллин Рашид Асхатович, автор
  • Ситдикова Гузель Фаритовна, автор
  • Хузахметова Венера Фаритовна, автор
  • Шакирзянова Анастасия Вячеславовна, автор
  • Библиографическое описание на языке оригинала Bukharaeva E. Homocysteine aggravates ROS-induced depression of transmitter release from motor nerve terminals: potential mechanism of peripheral impairment in motor neuron diseases associated with hyperhomocysteinemia / Bukharaeva E., Shakirzyanova A., Khuzakhmetova V., Sitdikova G., Giniatullin R. // Frontiers in Cellular Neuroscience. - 2015. - Vol.9.
    Аннотация Homocysteine (HCY) is a pro-inflammatory sulphur-containing redox active endogenous amino acid, which concentration increases in neurodegenerative disorders including amyotrophic lateral sclerosis (ALS). A widely held view suggests that HCY could contribute to neurodegeneration via promotion of oxidative stress. However, the action of HCY on motor nerve terminals has not been investigated so far. We previously reported that oxidative stress inhibited synaptic transmission at the neuromuscular junction, targeting primarily the motor nerve terminals. In the current study, we investigated the effect of HCY on oxidative stress-induced impairment of transmitter release at the mouse diaphragm muscle. The mild oxidant H2O2 decreased the intensity of spontaneous quantum release from nerve terminals (measured as the frequency of miniature endplate potentials, MEPPs) without changes in the amplitude of MEPPs, indicating a presynaptic effect. Pre-treatment with HCY for 2 h only slightly affected
    Ключевые слова amyotrophic lateral sclerosis, neuromuscular junction, homocysteine, oxidative stress, NMDA receptors
    Название журнала Frontiers in Cellular Neuroscience
    URL http://journal.frontiersin.org/article/10.3389/fncel.2015.00391/full
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