Форма представления | Статьи в зарубежных журналах и сборниках |
Год публикации | 2015 |
Язык | русский |
|
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 |
Пожалуйста, используйте этот идентификатор, чтобы цитировать или ссылаться на эту карточку |
https://repository.kpfu.ru/?p_id=117013 |
Файлы ресурса | |
|
Полная запись метаданных |
Поле DC |
Значение |
Язык |
dc.contributor.author |
Бухараева Элля Ахметовна |
ru_RU |
dc.contributor.author |
Гиниатуллин Рашид Асхатович |
ru_RU |
dc.contributor.author |
Ситдикова Гузель Фаритовна |
ru_RU |
dc.contributor.author |
Хузахметова Венера Фаритовна |
ru_RU |
dc.contributor.author |
Шакирзянова Анастасия Вячеславовна |
ru_RU |
dc.date.accessioned |
2015-01-01T00:00:00Z |
ru_RU |
dc.date.available |
2015-01-01T00:00:00Z |
ru_RU |
dc.date.issued |
2015 |
ru_RU |
dc.identifier.citation |
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. |
ru_RU |
dc.identifier.uri |
https://repository.kpfu.ru/?p_id=117013 |
ru_RU |
dc.description.abstract |
Frontiers in Cellular Neuroscience |
ru_RU |
dc.description.abstract |
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
|
ru_RU |
dc.language.iso |
ru |
ru_RU |
dc.subject |
amyotrophic lateral sclerosis |
ru_RU |
dc.subject |
neuromuscular junction |
ru_RU |
dc.subject |
homocysteine |
ru_RU |
dc.subject |
oxidative stress |
ru_RU |
dc.subject |
NMDA
receptors |
ru_RU |
dc.title |
Homocysteine aggravates ROS-induced depression of transmitter release from motor nerve terminals: potential mechanism of peripheral impairment in motor neuron diseases associated with hyperhomocysteinemia |
ru_RU |
dc.type |
Статьи в зарубежных журналах и сборниках |
ru_RU |
|