KFU. Card publication. Homocysteine aggravates ROS-induced depression of transmitter release from motor nerve terminals: potential mechanism of peripheral impairment in motor neuron diseases associated with hyperhomocysteinemia

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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

Form of presentation

Articles in international journals and collections

Year of publication

2015

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Authors, employees of KFU

Bukharaeva Ellya Akhmetovna, author

Giniatullin Rashid Askhatovich, author

Sitdikova Guzel Faritovna, author

Khuzakhmetova Venera Faritovna, author

Shakirzyanova Anastasiya Vyacheslavovna, author

Bibliographic description in the original language

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.

Annotation

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

Keywords

amyotrophic lateral sclerosis, neuromuscular junction, homocysteine, oxidative stress, NMDA receptors

The name of the journal

Frontiers in Cellular Neuroscience

URL

http://journal.frontiersin.org/article/10.3389/fncel.2015.00391/full

Please use this ID to quote from or refer to the card

https://repository.kpfu.ru/eng/?p_id=117013&p_lang=2

Resource files

File name	Size (MB)	Format
Homocysteine_aggravate.pdf	0,68	pdf	show / download

Full metadata record

Field DC	Value	Language
dc.contributor.author	Bukharaeva Ellya Akhmetovna	ru_RU
dc.contributor.author	Giniatullin Rashid Askhatovich	ru_RU
dc.contributor.author	Sitdikova Guzel Faritovna	ru_RU
dc.contributor.author	Khuzakhmetova Venera Faritovna	ru_RU
dc.contributor.author	Shakirzyanova Anastasiya Vyacheslavovna	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/eng/?p_id=117013&p_lang=2	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	Articles in international journals and collections	ru_RU