Форма представления | Статьи в зарубежных журналах и сборниках |
Год публикации | 2020 |
Язык | русский |
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Гайнутдинов Азат Робертович, автор
Мухтаров Марат Рахимзянович, автор
Хазипов Рустем Нариманович, автор
Юзекаева Эльвира Разилевна, автор
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Библиографическое описание на языке оригинала |
Juzekaeva, E., Gainutdinov, A., Mukhtarov, M., & Khazipov, R. (2020). Reappraisal of anoxic spreading depolarization as a terminal event during oxygen–glucose deprivation in brain slices in vitro. Scientific Reports, 10(1), 18970. https://doi.org/10.1038/s41598-020-75975-w
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Аннотация |
Scientific Reports | |
Ключевые слова |
brain ischemia, hypoxia, edema, swelling, cortex, anoxic depolarization, spreading cortical depression, barrel cortex, barrel, optical intrinsic
signals, silicone probes, electrophysiology |
Название журнала |
Scientific Reports |
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Пожалуйста, используйте этот идентификатор, чтобы цитировать или ссылаться на эту карточку |
https://repository.kpfu.ru/?p_id=267210 |
Полная запись метаданных |
Поле DC |
Значение |
Язык |
dc.contributor.author |
Гайнутдинов Азат Робертович |
ru_RU |
dc.contributor.author |
Мухтаров Марат Рахимзянович |
ru_RU |
dc.contributor.author |
Хазипов Рустем Нариманович |
ru_RU |
dc.contributor.author |
Юзекаева Эльвира Разилевна |
ru_RU |
dc.date.accessioned |
2020-01-01T00:00:00Z |
ru_RU |
dc.date.available |
2020-01-01T00:00:00Z |
ru_RU |
dc.date.issued |
2020 |
ru_RU |
dc.identifier.citation |
Juzekaeva, E., Gainutdinov, A., Mukhtarov, M., & Khazipov, R. (2020). Reappraisal of anoxic spreading depolarization as a terminal event during oxygen–glucose deprivation in brain slices in vitro. Scientific Reports, 10(1), 18970. https://doi.org/10.1038/s41598-020-75975-w
|
ru_RU |
dc.identifier.uri |
https://repository.kpfu.ru/?p_id=267210 |
ru_RU |
dc.description.abstract |
Scientific Reports | |
ru_RU |
dc.description.abstract |
Anoxic spreading depolarization (aSD) has been hypothesized as a terminal event during oxygen–
glucose deprivation (OGD) in submerged cortical slices in vitro. However, mechanical artifacts caused
by aSD-triggered edema may introduce error in the assessment of neuronal viability. Here, using
continuous patch-clamp recordings from submerged rat cortical slices, we first confirmed that vast
majority of L4 neurons permanently lost their membrane potential during OGD-induced aSD. In some
recordings, spontaneous transition from whole-cell to out-side out configuration occurred during or
after aSD, and only a small fraction of neurons survived aSD with reperfusion started shortly after
aSD. Secondly, to minimize artifacts caused by OGD-induced edema, cells were short-term patched
following OGD episodes of various duration. Nearly half of L4 cells maintained membrane potential
and showed the ability to spike-fire if reperfusion started less than 10 min after aSD. The probability
of finding live neurons progressively decreased at longer reperfusion delays at a rate of about 2%
per minute. We also found that neurons in L2/3 show nearly threefold higher resistance to OGD than
neurons in L4. Our results suggest that in the OGD ischemia model, aSD is not a terminal event, and
that the “commitment point” of irreversible damage occurs at variable delays, in the range of tens of
minutes, after OGD-induced aSD in submerged cortical slices. |
ru_RU |
dc.language.iso |
ru |
ru_RU |
dc.subject |
brain ischemia |
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dc.subject |
hypoxia |
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dc.subject |
edema |
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dc.subject |
swelling |
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dc.subject |
cortex |
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dc.subject |
anoxic depolarization |
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dc.subject |
spreading cortical depression |
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dc.subject |
barrel cortex |
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dc.subject |
barrel |
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dc.subject |
optical intrinsic
signals |
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dc.subject |
silicone probes |
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dc.subject |
electrophysiology |
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dc.title |
Reappraisal of anoxic spreading depolarization as a terminal event during oxygen–glucose deprivation in brain slices in vitro |
ru_RU |
dc.type |
Статьи в зарубежных журналах и сборниках |
ru_RU |
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