当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > Treadmill running attenuates neonatal hypoxia induced adult depressive symptoms and promoted hippocampal neural stem cell differentiation via modulating AMPK-mediated mitochondrial functions.

Treadmill running attenuates neonatal hypoxia induced adult depressive symptoms and promoted hippocampal neural stem cell differentiation via modulating AMPK-mediated mitochondrial functions.

Abstract：

:Neonatal hypoxia can induce the persisting brain dysfunctions and subsequently result in the behavioral abnormalities in adulthood. Improving mitochondrial functions were suggested as the effective strategy for brain functional recovery. In this study, we tested the effects of physical exercise, a well-established way benefits mitochondrion, for its functions to prevent hypoxia induced adult behavioral dysfunctions and the underlying molecular mechanism. Mice was induced with hypoxia and treadmill running were then administrated until the adulthood. The treadmill running resulted in the improved behavioral performance in depressive and anxiety tests together with the enhancement of hippocampal neurogenesis. We then detected treadmill running restored the mitochondrial morphology in adult neural stem cells (NSCs) as well as the ATP production in hippocampal tissue. In addition, activity of AMPK, which playing key roles in regulating mitochondrial functions, was also elevated by treadmill running. Blockage of AMPK with selective inhibitor compound C prohibited effects of treadmill running in attenuating neonatal hypoxia induced neurogenic impairment and antidepressant behavioral deficits in adulthood. In conclusion, treadmill running could prevent neonatal hypoxia induced adult antidepressant dysfunctions and neurogenic dampening via AMPK-mediated mitochondrial regulation.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Sun L,Ye R,Liang R,Xing F

doi

10.1016/j.bbrc.2019.12.036

subject

Has Abstract

pub_date

2020-03-05 00:00:00

pages

514-521

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(19)32356-3

journal_volume

523

pub_type

杂志文章

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