Schisandrae Chinensis Fructus inhibits behavioral deficits induced by sleep deprivation and chronic unpredictable mild stress via increased signaling of brain‐derived neurotrophic factor

Yan, Tingxu; Sun, Yingying; Xiao, Feng; Wu, Bo; Bi, Kaishun; He, Bin; Jia, Ying

doi:10.1002/ptr.6489

Cited by 26 publications

(14 citation statements)

References 30 publications

(37 reference statements)

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“…Considering that the main subcortical input of hippocampus is from the medial septum of the basal forebrain cholinergic system (Solari & Hangya 2018) and the septo‐hippocampal pathway, the main projection of medial septal neurons (Everitt & Robbins, 1997), is also important for processing of aversive information during fear conditioning (Calandreau, Jaffard, & Desmedt, 2007; Stepanichev, Lazareva, Tukhbatova, Salozhin, & Gulyaeva, 2014), there might be a possibility that sleep deprivation‐induced increase in basal forebrain BDNF might activate basal forebrain cholinergic neurons which further increased hippocampal BDNF expression and fear memory consolidation. Although recent research showed BDNF level in hippocampus was elevated by 12‐hr sleep deprivation (Yan et al, 2019), whether BDNF/TrkB (Y816)/ PLCγ(Y783) signaling in hippocampus was activated after sleep deprivation needs further confirmation.…”

Section: Discussionmentioning

confidence: 98%

“…It is tempting to relate the preservation of fear memory with the increased BDNF levels seen in the sleep deprived rats. Indeed, brain adaptive response after acute sleep deprivation has been confirmed in gene expression (Cirelli, Gutierrez, & Tononi, 2004), neurotransmitter release (Dash, Douglas, Vyazovskiy, Cirelli, & Tononi, 2009), and compensatory recruitment of different brain structures, such as hippocampus (Yan et al, 2019). In this context, and considering the pivotal functions of BDNF in memory consolidation, elevation of transcription of BDNF during acute sleep deprivation could play a modulating role of the fear memory process.…”

Section: Discussionmentioning

confidence: 99%

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Activation of brain‐derived neurotrophic factor signaling in the basal forebrain reverses acute sleep deprivation‐induced fear memory impairments

Zhang²,

et al. 2020

Brain and Behavior

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Introduction:The mechanisms underlying sleep deprivation-induced memory impairments and relevant compensatory signaling pathways remain elusive. We tested the hypothesis that increased brain-derived neurotrophic factor (BDNF) expression in the basal forebrain following acute sleep deprivation was a compensatory mechanism to maintain fear memory performance. Methods: Adult male Wistar rats were deprived of 6-hr total sleep from the beginning of the light cycle. The effects of sleep deprivation on BDNF protein expression and activation of downstream tropomyosin receptor kinase B (TrkB)/phospholipase C-γ1 (PLCγ1) signaling in the basal forebrain and fear memory consolidation were examined. BDNF or selective downstream TrkB receptor antagonist ANA-12 was further injected into the basal forebrain bilaterally to observe the changes in fear memory consolidation in response to modulation of the BDNF/TrkB signaling. Results: Six hours of sleep deprivation-induced both short-and long-term fear memory impairments. Increased BDNF protein expression and TrkB and PLCγ1 phosphorylation in the basal forebrain were observed after sleep deprivation. Microinjection of BDNF into the basal forebrain partly reversed fear memory deficits caused by sleep deprivation, which were accompanied by increased BDNF protein levels and TrkB/PLCγ1 activation. After ANA-12 microinjection, sleep deprivation-induced activation of the BDNF/TrkB pathway was inhibited and impairments of fear memory consolidation were further aggravated. Conclusions: Acute sleep deprivation induces compensatory increase of BDNF expression in the basal forebrain. Microinjection of BDNF into the basal forebrain mitigates the fear memory impairments caused by sleep deprivation by activating TrkB/ PLCγ1 signaling.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Activation of brain‐derived neurotrophic factor signaling in the basal forebrain reverses acute sleep deprivation‐induced fear memory impairments

Zhang²,

et al. 2020

Brain and Behavior

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“…In the present study, CUMS inhibited BDNF/TrkB/ERK/CREB signaling pathway, which was in accordance with the previous studies. [ 35–37 ] In contrast, chronic porphyran administration for 4 weeks reversed the inhibition of BDNF/TrkB/ERK/CREB pathway. Besides the neurotrophic signaling, we also evaluated the effects of porphyran on neurogenesis and spinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Antidepressant‐like Effects of Degraded Porphyran Isolated fromPorphyra haitanensis

Zhang

Cheng

et al. 2021

Molecular Nutrition Food Res

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Introduction Degraded porphyran is a bioactive polysaccharide extracted from Porphyra haitanensis (P. haitanensis). According to the previous studies, it produced anti‐inflammatory activity, but little is known about its effects on depression. Methods and Results As inflammation is one of the critical factors involved in the development of depression, this study aims to elucidate the potential antidepressant‐like effects of degraded porphyran. The results show that acute porphyran treatment decreased the immobility time in despair tests. In addition, subchronic porphyran administration reverses depressive‐like behaviors in lipopolysaccharide (LPS)‐treated mice. Meanwhile, porphyran inhibits NF‐κB/NLRP3 signaling, proinflammatory cytokine release, and microglial activation in the hippocampus. Moreover, chronic porphyran treatment activates hippocampal brain derived neurotrophic factor (BDNF)/TrkB/ERK/CREB signaling pathway in chronic unpredictable mild stress (CUMS) in mice. As a result, neurogenesis and spinogenesis are maintained. Conclusions The findings of the present study indicate that degraded porphyran intake provides a potential strategy for depression treatment, which is mediated by the inhibition of neuroinflammation and the enhancement of neurogenesis and spinogenesis in the central nervous systems.

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“…After these new neurons are generated, they proliferate, migrate, and differentiate and are subsequently integrated into the existing neuronal circuits to form synaptic connections [ 11 ]. Brain-derived neurotrophic factor (BDNF) is widely distributed in the brain and plays an important role in the survival, development, and growth of central neurons [ 12 ] and is involved in the regulation of neurogenesis [ 13 ]. Decreased BDNF levels and abnormal neurogenesis are associated with depressive symptoms and behaviors [ 14 , 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

Cryptotanshinone ameliorates CUS-induced depressive-like behaviors in mice

Wang

Zhai

Wang

et al. 2021

Translational Neuroscience

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Objectives Cryptotanshinone (CPT), a natural quinoid diterpene, isolated from Salvia miltiorrhiza, has shown various pharmacological properties. However, its effect on chronic unpredictable stress (CUS)-induced depression phenotypes and the underlying mechanism remain unclear. Therefore, the aim of this study was to investigate whether CPT could exert an antidepressant effect. Methods We investigated the effects of CPT in a CUS-induced depression model and explored whether these effects were related to the anti-inflammatory and neurogenesis promoting properties by investigating the expression levels of various signaling molecules at the mRNA and protein levels. Results Administration of CPT improved depression-like behaviors in CUS-induced mice. CPT administration increased the levels of doublecortin-positive cells and reversed the decrease in the expression levels of brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) signaling transduction, as well as the downstream functional proteins, phosphorylated extracellular regulated protein kinases (p-ERK), and cyclic adenosine monophosphate (cAMP)-response element-binding protein levels (p-CREB) in hippocampus. CPT treatment also inhibited the activation of microglia and suppressed M1 microglial polarization, while promoting M2 microglial polarization by monitoring the expression levels of arginase 1 (Arg-1) and inducible nitric oxide synthase (iNOS), and further inhibited the expression of proinflammatory cytokines, including interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α), and increased the expression of the anti-inflammatory cytokine IL-10 by regulating nuclear factor-κB (NF-κB) activation. Conclusions CPT relieves the depressive-like state in CUS-induced mice by enhancing neurogenesis and inhibiting inflammation through the BDNF/TrkB and NF-κB pathways and could therefore serve as a promising candidate for the treatment of depression.

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Schisandrae Chinensis Fructus inhibits behavioral deficits induced by sleep deprivation and chronic unpredictable mild stress via increased signaling of brain‐derived neurotrophic factor

Cited by 26 publications

References 30 publications

Activation of brain‐derived neurotrophic factor signaling in the basal forebrain reverses acute sleep deprivation‐induced fear memory impairments

Activation of brain‐derived neurotrophic factor signaling in the basal forebrain reverses acute sleep deprivation‐induced fear memory impairments

Antidepressant‐like Effects of Degraded Porphyran Isolated fromPorphyra haitanensis

Cryptotanshinone ameliorates CUS-induced depressive-like behaviors in mice

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