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Prenatal hypoxia induces premature aging accompanied by impaired function of the glutamatergic system in rat hippocampusстатья
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 12 января 2022 г.
- Авторы: Vetrovoy Oleg, Stratilov Viktor, Nimiritsky Peter, Makarevich Pavel, Tyulkova Ekaterina
- Журнал: Neurochemical Research
- Том: 46
- Номер: 3
- Год издания: 2021
- Издательство: Kluwer Academic/Plenum Publishers
- Местоположение издательства: United States
- Первая страница: 550
- Последняя страница: 563
- DOI: 10.1007/s11064-020-03191-z
- Аннотация: Prenatal hypoxia is among leading causes of progressive brain pathologies in postnatal life. This study aimed to analyzethe characteristics of the hippocampal glutamatergic system and behavior of rats in early (2 weeks), adult (3 months) andadvanced (18 months) postnatal ontogenesis after exposure to prenatal severe hypoxia (PSH, 180 Torr, 5% O2, 3 h) during thecritical period in the formation of the hippocampus (days 14–16 of gestation). We have shown an age-dependent progressivedecrease in the hippocampal glutamate levels, a decrease of the neuronal cell number in the CA1 hippocampal region, aswell as impairment of spatial long-term memory in the Morris water navigation task. The gradual decrease of glutamate wasaccompanied by decreased expression of the genes that mediate glutamate metabolism and recycling in the hippocampus.That deiciency apparently correlated with an increase of the metabotropic glutamate receptor type 1 (mGluR1) and synaptophysin expression. Generation of the lipid peroxidation products in the hippocampus of adult rats subjected to prenatalsevere hypoxia (PSH rats) was not increased compared to the control animals when tested in a model of glutamate excitotoxicity induced by severe hypoxia. This demonstrates that excessive glutamate sensitivity in PSH rats does not compensatefor glutamate deiciency. Our results show a signiicant contribution of the glutamate system dysfunction to age-associateddecrease of this mediator, cognitive decline, and early neuronal loss in PSH rats.
- Добавил в систему: Ветровой Олег Васильевич