Neuroplasticity and behavioral effects of fluoxetine after experimental stroke

Sun, Yefei; Sun, Xiaoyu; Qu, Huiling; Zhao, Shanshan; Xiao, Ting; Zhao, Chuansheng

doi:10.3233/rnn-170725

Cited by 16 publications

(13 citation statements)

References 104 publications

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“…DES and FLX have distinct mechanism of action, while the former inhibits NE reuptake 83,84 , the second selectively inhibits serotonin reuptake 85,86 . FLX effect in increasing neurogenesis is well grounded in the literature [87][88][89] . Interestingly, one study that measured neurogenesis based on specific cell types showed that FLX effects depend on the dorsoventral axis of the hippocampus 27 .…”

Section: Discussionmentioning

confidence: 89%

Pro-neurogenic effect of fluoxetine in the olfactory bulb is concomitant to improvements in social memory and depressive-like behavior of socially isolated mice

Medeiros

et al. 2020

Transl Psychiatry

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Although loneliness is a human experience, it can be estimated in laboratory animals deprived from physical contact with conspecifics. Rodents under social isolation (SI) tend to develop emotional distress and cognitive impairment. However, it is still to be determined whether those conditions present a common neural mechanism. Here, we conducted a series of behavioral, morphological, and neurochemical analyses in adult mice that underwent to 1 week of SI. We observed that SI mice display a depressive-like state that can be prevented by enriched environment, and the antidepressants fluoxetine (FLX) and desipramine (DES). Interestingly, chronic administration of FLX, but not DES, was able to counteract the deleterious effect of SI on social memory. We also analyzed cell proliferation, neurogenesis, and astrogenesis after the treatment with antidepressants. Our results showed that the olfactory bulb (OB) was the neurogenic niche with the highest increase in neurogenesis after the treatment with FLX. Considering that after FLX treatment social memory was rescued and depressive-like behavior decreased, we propose neurogenesis in the OB as a possible mechanism to unify the FLX ability to counteract the deleterious effect of SI.

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Section: Discussionmentioning

confidence: 89%

Pro-neurogenic effect of fluoxetine in the olfactory bulb is concomitant to improvements in social memory and depressive-like behavior of socially isolated mice

Medeiros

et al. 2020

Transl Psychiatry

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“…When the neuronal injury is mild, the FLU treatment could improve the cellular neuroplasticity and microtubule plasticity to improve antidepressant effect. Many studies [36, 51,52] have confirmed this view. However, when the neuronal injury is severe, FLU alone treatment would aggravate cellular neuroplasticity and microtubule plasticity, which may be one of the biological bases of depression recurrence.…”

Section: Implications Of Flu Treatment For Depressionmentioning

confidence: 80%

Fluoxetine treatment for more than 2 days decreases the cellular neuroplasticity and microtubule plasticity in differentiated PC12 cells

Wu¹,

Wang²,

Wang³

et al. 2019

Preprint

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Background: Recent studies indicate that antidepressants treatment restores neuroplasticity. But some researchers claimed that antidepressants, including fluoxetine (FLU), may exacerbate neuroplasticity, which is contradictory and rarely studied. Since almost all of those studies treated with drugs for 1 to 2 days as treatment models of antidepressants, it is possible that FLU treatments for longer periods would have opposite effects on neuroplasticity. Results: In the present study, we examined the effects of FLU treatment up to 3 days on the cellular neuroplasticity and microtubule plasticity in PC12 cells. The cell viability of cells happened a small decease at 2 days (93.5±3.5%), followed by highly significant decreases at 3 days (71.4±4.4%). As report previously, cellular neuroplasticity was significantly upregulated with FLU treatment at 1 day, but that was inhibited FLU treatment at 3 days. Similarly, the expression of tubulin, which is microtubulin plasticity marker, was also upregulated with FLU treatment at 1 day. But it decreased significantly in cells treated with FLU at 3 days. Furthermore, we found tubulin interacted with CRMP2, which accelerated to cellular neuroplasticity, and the regulation of CRMP2 activity influenced microtubule plasticity. Conclusions: The results demonstrate that cellular neuroplasticity and microtubule plasticity were increased with FLU treatment at 1 day, but treatment with FLU for more than 2 days has opposite effect on them. The reduction in cellular neuroplasticity andmicrotubule plasticity with FLU treatment for more than 2 days might be involved in some aspects of the drugs’ therapeutic effects on depression.

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“…Understanding the role of Notch2 signaling in stroke may provide insights on development of new therapeutics [43]. The brain undergoes self-repair by producing new neurons and has the ability to compensate for the loss of function after stroke [44]. NEDD9 (Neuronal precursor cell-expressed, developmentally down-regulated gene) was initially identi ed in mouse central nervous system [45,46].…”

Section: Discussionmentioning

confidence: 99%

Hub Genes of Stroke Identified by Weighted Gene Co-expression Network Analysis

Zhai

et al. 2020

Preprint

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BACKGROUD: Microarray-based gene expression profiling is widely used in biomedical research. Weighted gene co-expression network analysis (WGCNA) links microarray data directly to clinical traits and identifies rules for predicting pathological stage and prognosis of disease.WGCNA is useful in understandingmany biological processes. Stroke is a common disease worldwide, however, molecular mechanisms of its pathogenesis are largely unknown. The aim of this study was to construct gene co-expression networks for identification of key modules and hub genes associated with stroke pathogenesis.METHODS: Gene microarray expression profiles of stroke samples were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were screened by the limma package in R software. WGCNA was used to construct free-scale gene co-expression networks to explore the associations between gene sets and clinical features, and to identify key modules and hub genes. Subsequently, functional enrichment analyses were performed. Further, receiver operating characteristic (ROC) curve analysis was carried out to validate expression of hub genes and literature validation was performed as well.RESULTS: A total of 11,747 most variant genes were used for co-expression network construction. Pink and yellow modules were significantly correlated to stroke pathogenesis. Functional enrichment analysis showed that the pink module was mainly involved in regulation of neuron regeneration, and repair of DNA damage.On the other hand, yellow module was mainly enriched in ion transport system dysfunction which was correlated with neuron death. A total of eight hub genes (PRR11, NEDD9, Notch2, RUNX1-IT1, ANP32A-IT1, ASTN2, SAMHD1 and STIM1) were identified and validated at transcriptional levels and through existing literature.CONCLUSION: The eight hub genes (PRR11, NEDD9, Notch2, RUNX1-IT1, ANP32A-IT1, ASTN2, SAMHD1 and STIM1) identified in the study are potentialbiomarkers and therapeutic targets for effective diagnosis and treatment of stroke.

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Neuroplasticity and behavioral effects of fluoxetine after experimental stroke

Cited by 16 publications

References 104 publications

Pro-neurogenic effect of fluoxetine in the olfactory bulb is concomitant to improvements in social memory and depressive-like behavior of socially isolated mice

Pro-neurogenic effect of fluoxetine in the olfactory bulb is concomitant to improvements in social memory and depressive-like behavior of socially isolated mice

Fluoxetine treatment for more than 2 days decreases the cellular neuroplasticity and microtubule plasticity in differentiated PC12 cells

Hub Genes of Stroke Identified by Weighted Gene Co-expression Network Analysis

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