Maternal stress induced autophagy dysfunction and immune activation in the hippocampus of adolescence rat pups
3
Issued Date
2022-04-01
Resource Type
ISSN
08910618
eISSN
18736300
Scopus ID
2-s2.0-85125717701
Pubmed ID
35257877
Journal Title
Journal of Chemical Neuroanatomy
Volume
121
Rights Holder(s)
SCOPUS
Bibliographic Citation
Journal of Chemical Neuroanatomy Vol.121 (2022)
Suggested Citation
Surakul P. Maternal stress induced autophagy dysfunction and immune activation in the hippocampus of adolescence rat pups. Journal of Chemical Neuroanatomy Vol.121 (2022). doi:10.1016/j.jchemneu.2022.102085 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/87565
Title
Maternal stress induced autophagy dysfunction and immune activation in the hippocampus of adolescence rat pups
Author(s)
Author's Affiliation
Other Contributor(s)
Abstract
Maternal stress (MS) has long-term effects on fetal brain development and consequently increases the risk of neuropsychiatric diseases in the offspring, however, the mechanism that links between early life stress and subsequent neuropsychiatric diseases is still not clear. It is well known that both neuroinflammation and autophagy dysfunction contributes to the pathology of psychiatric disorders. We hypothesized that MS might alter autophagy function and activate the neuroimmune response in the pup's brain. To test this hypothesis, we investigated the effects of MS on the expression of the autophagy biomarker and neuroimmune response in the hippocampus of rat pups. Results revealed that MS-induced a long-term decrease of LC3B-II throughout the postnatal periods, together with an increase of IL-6 and IL-10 in the hippocampus of rat pups during adolescence. These changes lasted at least until adulthood. Results from the In vitro studies showed that a partially toxic dose of corticosterone (CORT) induced a significant decrease of LC3B-II, together with an increase of IL-6 and IL-10, in the SH-SY5Y cells. Moreover, suppression of autophagy by mycophenolic acid (MPA) leads to an increased IL-6 and IL-10 expression in the CORT-treated SH-SY5Y cells. Findings suggested that CORT decreased autophagy dysfunction could activate neuroimmune response in the SH-SY5Y cells. Results from this study provides initial evidence for the relationship between stress hormone, autophagy dysfunction, and neuroimmune activation, which may be the linking mechanism between early-life stress and subsequent neuropsychiatric disorders.