Maternal sleep deprivation inhibits hippocampal neurogenesis associated with inflammatory response in young offspring rats

Zhao, Qiuying; Peng, Cheng; Wu, Xiaohui; Chen, Yubo; Wang, Cheng; You, Zhang

doi:10.1016/j.nbd.2014.04.008

Cited by 80 publications

(91 citation statements)

References 71 publications

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“…The total numbers of BrdU + cells and BrdU + /DCX + cells in MSD offspring were smaller than that of the control. This showed that hippocampal neurogenesis is reduced in the DG in young rats by MSD, which conforms with the findings of our previous research26. These results support the concept that prenatal stress can induce lasting and profound changes in the offspring, potently inhibiting neurogenesis10.…”

Section: Discussionsupporting

confidence: 92%

“…Thus, minocycline is a useful tool to investigate the mechanisms underlying microglial polarization and the pathogeneses of many diseases accompanied by microglial activation2225. Previous studies from our laboratory indicated that MSD increased the number of Iba1 + (Ionized calcium-binding adaptor protein-1) cells and decreased hippocampal neurogenesis, induced imbalance between pro- and anti-inflammatory cytokines in the brain, and resulted in cognitive deficits and behavioral abnormalities in young offspring26. Nevertheless, the mechanism of microglial activation and dysregulation of cytokine signaling pathway involved in the precipitation of postnatal brain and behavioral pathology still remains to be explored.…”

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confidence: 97%

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Phenotypic dysregulation of microglial activation in young offspring rats with maternal sleep deprivation-induced cognitive impairment

Zhao

Xie

Fan

et al. 2015

Sci Rep

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Despite the potential adverse effects of maternal sleep deprivation (MSD) on physiological and behavioral aspects of offspring, the mechanisms remain poorly understood. The present study was intended to investigate the roles of microglia on neurodevelopment and cognition in young offspring rats with prenatal sleep deprivation. Pregnant Wistar rats received 72 h sleep deprivation in the last trimester of gestation, and their prepuberty male offspring were given the intraperitoneal injection with or without minocycline. The results showed the number of Iba1+ microglia increased, that of hippocampal neurogenesis decreased, and the hippocampus-dependent spatial learning and memory were impaired in MSD offspring. The classical microglial activation markers (M1 phenotype) IL-1β, IL-6, TNF-α, CD68 and iNOS were increased, while the alternative microglial activation markers (M2 phenotype) Arg1, Ym1, IL-4, IL-10 and CD206 were reduced in hippocampus of MSD offspring. After minocycline administration, the MSD offspring showed improvement in MWM behaviors and increase in BrdU+/DCX+ cells. Minocycline reduced Iba1+ cells, suppressed the production of pro-inflammatory molecules, and reversed the reduction of M2 microglial markers in the MSD prepuberty offspring. These results indicate that dysregulation in microglial pro- and anti-inflammatory activation is involved in MSD-induced inhibition of neurogenesis and impairment of spatial learning and memory.

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Section: Discussionsupporting

confidence: 92%

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confidence: 97%

Phenotypic dysregulation of microglial activation in young offspring rats with maternal sleep deprivation-induced cognitive impairment

Zhao

Xie

Fan

et al. 2015

Sci Rep

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“…Evidence has suggested that inflammatory response induced by maternal stress is an important factor for impairing hippocampal structure and hippocampus-dependent behavior in offspring [33,34]. Immune stress during pregnancy has been reported to be associated with impaired hippocampal function in the offspring [35,36].…”

Section: Discussionmentioning

confidence: 99%

Maternal immune activation increases seizure susceptibility in juvenile rat offspring

Yin

Zhang

et al. 2015

Epilepsy & Behavior

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“…The SPT was performed as described previously [25] , with minor modification. Briefly, 72 h before the test, mice were habituated to drink 1% sucrose solution, followed by depri-vation of water and food for 12 h. Then, mice were free to access either of two bottles containing 1% sucrose solution or water.…”

Section: Sucrose Preference Test (Spt) and Body Weight Measurementmentioning

confidence: 99%

Salvianolic acid B ameliorates depressive-like behaviors in chronic mild stress-treated mice: involvement of the neuroinflammatory pathway

Zhang

Feng

et al. 2016

Acta Pharmacol Sin

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Aim: Major depressive disorder (MDD) is a debilitating mental disorder associated with dysfunction of the neurotransmitterneuroendocrine system and neuroinflammatory responses. Salvianolic acid B (SalB) has shown a variety of pharmacological activities, including anti-inflammatory, antioxidant and neuroprotective effects. In this study, we examined whether SalB produced antidepressantlike actions in a chronic mild stress (CMS) mouse model, and explored the mechanisms underlying the antidepressant-like actions of SalB. Methods: Mice were subjected to a CMS paradigm for 6 weeks. In the last 3 weeks the mice were daily administered SalB (20 mg·kg -1 ·d -1 , ip) or a positive control drug imipramine (20 mg·kg -1 ·d -1 , ip). The depressant-like behaviors were evaluated using the sucrose preference test, the forced swimming test (FST), and the tail suspension test (TST). The gene expression of cytokines in the hippocampus and cortex was analyzed with RT-PCR. Plasma corticosterone (CORT) and cerebral cytokines levels were assayed with an ELISA kit. Neural apoptosis and microglial activation in brain tissues were detected using immunofluorescence staining. Results: Administration of SalB or imipramine reversed the reduced sucrose preference ratio of CMS-treated mice, and significantly decreased their immobility time in the FST and TST. Administration of SalB significantly decreased the expression of pro-inflammatory cytokines IL-1β and TNF-α, and markedly increased the expression of anti-inflammatory cytokines IL-10 and TGF-β in the hippocampus and cortex of CMS-treated mice, and normalized their elevated plasma CORT levels, whereas administration of imipramine did not significantly affect the imbalance between pro-and anti-inflammatory cytokines in the hippocampus and cortex of CMS-treated mice. Finally, administration of SalB significantly decreased CMS-induced apoptosis and microglia activation in the hippocampus and cortex, whereas administration of imipramine had no significant effect on CMS-induced apoptosis and microglia activation in the hippocampus and cortex. Conclusion: SalB exerts potent antidepressant-like effects in CMS-induced mouse model of depression, which is associated with the inhibiting microglia-related apoptosis in the hippocampus and the cortex.

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Maternal sleep deprivation inhibits hippocampal neurogenesis associated with inflammatory response in young offspring rats

Cited by 80 publications

References 71 publications

Phenotypic dysregulation of microglial activation in young offspring rats with maternal sleep deprivation-induced cognitive impairment

Phenotypic dysregulation of microglial activation in young offspring rats with maternal sleep deprivation-induced cognitive impairment

Maternal immune activation increases seizure susceptibility in juvenile rat offspring

Salvianolic acid B ameliorates depressive-like behaviors in chronic mild stress-treated mice: involvement of the neuroinflammatory pathway

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