Profiling changes in cortical astroglial cells following chronic stress

Simard, Stephanie; Coppola, Gianfilippo; Rudyk, Chris; Hayley, Shawn; McQuaid, Robyn J.; Salmaso, Natalina

doi:10.1038/s41386-018-0105-x

Cited by 44 publications

(45 citation statements)

References 72 publications

(63 reference statements)

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“…Stress and depression can enhance PNN deposition and also render PNNs resistant to proteolysis (Pantazopoulos et al, 2015;Riga et al, 2017;Simard et al, 2018). Both processes can increase overall PNN levels.…”

Section: Schematic; Hypothetical Changes In Pnn Deposition and Mmp-9 mentioning

confidence: 99%

Venlafaxine stimulates an MMP-9-dependent increase in excitatory/inhibitory balance in a stress model of depression

Alaiyed

McCann

Mahajan

et al. 2019

Preprint

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AbstractEmerging evidence suggests that there is a reduction in overall cortical excitatory to inhibitory balance in major depressive disorder (MDD), which afflicts approximately 14-20% of individuals. Reduced pyramidal cell arborization occurs with stress and MDD, and may diminish excitatory neurotransmission. Enhanced deposition of perineuronal net (PNN) components also occurs with stress. Since parvalbumin-expressing interneurons are the predominant cell population that is enveloped by PNNs, which enhance their ability to release GABA, excess PNN deposition likely increases pyramidal cell inhibition. In the present study we investigate the potential for matrix metalloprotease-9 (MMP-9), an endopeptidase secreted in response to neuronal activity, to contribute to the antidepressant efficacy of venlafaxine, a serotonin/norepinephrine reuptake inhibitor. Chronic venlafaxine increases MMP-9 levels in murine cortex, and increases both pyramidal cell arborization and PSD-95 expression in the cortex of wild-type but not MMP-9 null mice. We have previously shown that venlafaxine reduces PNN deposition and increases the power of ex vivo gamma oscillations in conventionally-housed mice. Gamma power is increased with pyramidal cell disinhibition and with remission from MDD. Herein we observe that PNN expression is increased in a corticosterone-induced stress model of disease and reduced by venlafaxine. As compared to mice that receive concurrent venlafaxine, corticosterone treated mice also display reduced ex vivo gamma power and impaired working memory. Autopsy-derived prefrontal cortex samples show elevated MMP-9 levels in anti-depressant treated MDD patients as compared to controls. These preclinical and postmortem findings highlight a link between extracellular matrix regulation and MDD.

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Section: Schematic; Hypothetical Changes In Pnn Deposition and Mmp-9 mentioning

confidence: 99%

Venlafaxine stimulates an MMP-9-dependent increase in excitatory/inhibitory balance in a stress model of depression

Alaiyed

McCann

Mahajan

et al. 2019

Preprint

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“…SYNPO2 was demonstrated to closely associate with cognitive development in mice brain [59]. Chronic variable stress in mice induced signi cantly down-regulation of SYNPO2 which was necessary for synaptic plasticity, learning and memory [59]. Although there is less evidence to link caffeine consumption to SYNPO2 expression change, our result suggests that caffeine may in uence the intelligence by affecting the expression of SYNPO2 in human brain.…”

Section: Discussionmentioning

confidence: 70%

“…The GWASdb SNP-Phenotype association dataset showed that SYNPO2 was associated with the schizophrenia phenotype in GWAS datasets [58]. SYNPO2 was demonstrated to closely associate with cognitive development in mice brain [59]. Chronic variable stress in mice induced signi cantly down-regulation of SYNPO2 which was necessary for synaptic plasticity, learning and memory [59].…”

Section: Discussionmentioning

confidence: 99%

Genome-wide environmental interaction analysis identifies dietary habit related risk loci for depression and intelligence in UK Biobank

Cheng¹,

Chu²,

Wen³

et al. 2020

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Background Dietary habits have considerable impact on brain development and mental health. Our aim is to explore the possible association of dietary habits with depression and intelligence. Methods A total of 814 independent loci from a genome-wide association study (GWAS) of dietary habits were utilized to calculate the individual polygenic risk score (PRS) for 143 dietary habits related traits. The individual genotype data were obtained from UK Biobank cohort. Regression analyses were then conducted to evaluate the possible association of dietary habits with depression (including 153,549 subjects) and intelligence (including 160,121 subjects), respectively. Using dietary habits related PRSs as covariates, PLINK 2.0 was utilized to detect the SNP × dietary habit interaction effect on the risks of depression and intelligence, respectively. Results We detected 32 and 41 candidate dietary habits related traits for depression and intelligence, respectively, such as never eat sugar vs. no sugar restrictions (P = 1.09 × 10− 2) for depression, and coffee type: decaffeinated vs. any other (P = 8.77 × 10− 3) for intelligence. We also detected 22 common dietary habits related traits shared by depression and intelligence, such as red wine glasses per month (Pdepression = 8.75 × 10− 3, Pintelligence = 3.35 × 10− 19), and overall alcohol intake (Pdepression = 3.60 × 10− 2, Pintelligence = 8.31 × 10− 8). Interaction analysis of depression detected OLFM1 with 9 significant SNPs interacted with champagne/white wine glasses per month. Interaction analysis of intelligence detected SYNPO2 with 3 significant SNPs interacted with coffee type: decaffeinated vs. any other. Conclusions Our study results provide novel useful information for understanding how eating habits affecting the intelligence and the risk of depression.

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“…In order to conceptualize the overall anxiety and depressive phenotype, we included a total “emotionality score” that we have previously employed and was first described by the Sibille laboratory [ 24 , 27 ]; a significant increase in emotionality was induced by stress, which was reduced in fluoxetine-treated stressed WT mice ( Fig 5A ). No effect of fluoxetine was seen in FGF2KOs.…”

Section: Resultsmentioning

confidence: 99%

“…The emotionality score was derived as previously described in Guilloux (2011) [ 24 ]. Z scores were calculated for each test and normalized for locomotor behavior, as appropriate.…”

Section: Methodsmentioning

confidence: 99%

Fibroblast growth factor 2 is necessary for the antidepressant effects of fluoxetine

et al. 2018

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Previous research has shown that fibroblast growth factor 2 protein (FGF2) can act as an anxiolytic and anti-depressive agent in rodents. Levels of hippocampal FGF2 and FGF2 receptors are decreased in post-mortem brains of individuals with mood disorders. No changes in FGF2 were noted in the post-mortem brains of individuals with mood disorders that were successfully treated with anti-depressant medication prior to death. Mutations in the FGF2 gene in humans have been shown to predict non-responsiveness to the therapeutic effects of selective serotonin reuptake inhibitors (SSRIs). These findings suggest that FGF2 may potentially be a target of and/or required for the therapeutic effects of antidepressant medications. To test this, we employed a rodent model of depressive behaviour, chronic variable stress (CVS) in conjunction with antidepressant treatment (fluoxetine) in wild-type (WT) and FGF2 knockout mice (FGF2KO) and examined depressive and anxiety behaviors. Results showed that fluoxetine reversed the effects of CVS on depressive and anxiety behaviours in wild-type mice only, suggesting that the FGF2 gene is indeed necessary for the therapeutic effects of fluoxetine. Interestingly, CVS decreased hippocampal FGF2 levels and fluoxetine partially reversed this effect. Because FGF2 has been previously shown to modify HPA activity through hippocampal glucocorticoid receptors (GR), we examined levels of glucocorticoid receptors and found a decrease in GR in response to CVS, with a further decrease in FGF2KO. No effect of fluoxetine on GR was observed in either WT or FGF2KO mice. This suggests that further changes in glucocorticoid receptors are not necessary for the anti-depressant effects of fluoxetine in WT mice, although decreased glucocorticoid receptors in response to FGF2 deletion may preclude the therapeutic actions of fluoxetine in FGF2KO. Whether astroglia, astroglial functions, or HPA changes are the downstream target of FGF2-mediated changes induced by fluoxetine remains to be determined, however, the current study reaffirms the potential of FGF2 as a novel therapeutic target in the treatment of depression and anxiety disorders.

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Profiling changes in cortical astroglial cells following chronic stress

Cited by 44 publications

References 72 publications

Venlafaxine stimulates an MMP-9-dependent increase in excitatory/inhibitory balance in a stress model of depression

Venlafaxine stimulates an MMP-9-dependent increase in excitatory/inhibitory balance in a stress model of depression

Genome-wide environmental interaction analysis identifies dietary habit related risk loci for depression and intelligence in UK Biobank

Fibroblast growth factor 2 is necessary for the antidepressant effects of fluoxetine

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