Acute hypoxia exposure following prenatal stress impairs hippocampus and novelty-seeking behavior in adolescent rats
Yükleniyor...
Dosyalar
Tarih
2021
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
WILEY
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Objectives: The present study aimed to investigate the effects of acute hypoxia exposure following prenatal stress on the novelty-seeking behavior and hippocampus of adolescent rats. Methods: The offspring were divided into prenatal stress (PS) and non-stress (NS) groups. Both groups were exposed to hypoxia on postnatal day 10 (P10) while control groups were undisturbed. Novel object recognition task was performed in each group. Next, brains were collected to examine hippocampus via immunohistochemical and biochemical studies on postnatal day 35 (P35). Results: PS decreased novelty discrimination and synaptophysin (SYN) expressions both in CA1 & CA3 of the hypoxia group prominently (p<0.05). Nestin-expressing cells were reduced while vascular endothelial growth factor (VEGF) expression was enhanced in the subgranular zone (SGZ) of PS-hypoxia group (p<0.05). VEGF enhancement triggered angiogenesis in the CA1&CA3 significantly (p<0.05). PS also increased thiobarbituric acid reactive substances (TBARS) levels in the hypoxia group as a result of oxidative stress (p<0.05). Conclusion: These findings demonstrated that PS exacerbates neurodevelopmental deficits in the hippocampus of acute hypoxia-induced offspring in adolescence.
Açıklama
Anahtar Kelimeler
Hippocampus, Hypoxia, Novelty-seeking, Prenatal Stress
Kaynak
International Journal of Developmental Neuroscience
WoS Q Değeri
Q3
Scopus Q Değeri
N/A
Cilt
Sayı
Künye
Çelik, K., Bilim, P., Garip, G., Durmaz, B., Yildirim Sözmen, E., & Baka, M. (2021). Acute hypoxia exposure following prenatal stress impairs hippocampus and novelty-seeking behavior in adolescent rats. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 10.1002/jdn.10162. Advance online publication.