Differential Peripheral Proteomic Biosignature of Fluoxetine Response in a Mouse Model of Anxiety/Depression

Mendez‐David, Indira; Boursier, Céline; Domergue, Valérie; Colle, Romain; Falissard, Bruno; Corruble, Emmanuelle; Gardier, Alain M.; Guilloux, Jean‐Philippe; David, Denis J.

doi:10.3389/fncel.2017.00237

Cited by 27 publications

(31 citation statements)

References 59 publications

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“…Föcking, M et al found that AP2B1 was up‐regulated in the brain regions of patients with schizophrenia (Focking et al, ). It is worth mentioning that AP2B1 is up‐regulated in a mouse model of anxiety/depression and associated with antidepressant drug response (Mendez‐David et al, ). In this study, AP2B1 was down‐regulated in the blood of MDD and the expression pattern was validated by qRT‐PCR.…”

Section: Discussionmentioning

confidence: 99%

Seeking for potential pathogenic genes of major depressive disorder in the Gene Expression Omnibus database

Feng¹,

Zhou²,

Gao³

et al. 2019

Asia-Pacific Psychiatry

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Introduction: Major depressive disorder (MDD) is one of the most common mental disorders worldwide. The aim of this study was to identify potential pathological genes in MDD. Methods: We searched and downloaded gene expression data from the Gene Expression Omnibus database to identify differentially expressed genes (DEGs) in MDD. Then, Kyoto Encyclopedia of Genes and Genomes pathway, Gene Ontology analysis, and protein-protein interaction (PPI) network were applied to investigate the biological function of identified DEGs. The quantitative real-time polymerase chain reaction and a published dataset were used to validate the result of bioinformatics analysis. Results: A total of 514 DEGs were identified in MDD. In the PPI network, some hub genes with high degrees were identified, such as EEF2, RPL26L1, RPLP0, PRPF8, LSM3, DHX9, RSRC1, and AP2B1. The result of in vitro validation of RPL26L1, RSRC1, TOMM20L, RPLPO, PRPF8, AP2B1, STIP1, and C5orf45 was consistent with the bioinformatics analysis. Electronic validation of C5orf45, STIP1, PRPF8, AP2B1, and SLC35E1 was consistent with the bioinformatics analysis. Discussion: The deregulated genes could be used as potential pathological factors of MDD. In addition, EEF2, RPL26L1, RPLP0, PRPF8, LSM3, DHX9, RSRC1, and AP2B1 might be therapeutic targets for MDD. K E Y W O R D S drug target, gene expression, in vitro validation, major depressive disorder, protein-protein interaction network

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Section: Discussionmentioning

confidence: 99%

Seeking for potential pathogenic genes of major depressive disorder in the Gene Expression Omnibus database

Feng¹,

Zhou²,

Gao³

et al. 2019

Asia-Pacific Psychiatry

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“…While these data are consistent with a decreased hedonic drive, they may also have resulted from anxiety-induced suppression of feeding ( 84 ). In fact, a recent study shows that administration of anxiolytic drug fluoxetine results in a recovery of feeding behavior in a corticosterone-induced rodent model of anxiety ( 85 ). Future studies of GEPR-3s investigating changes in reward and learning behaviors under conditions of similarly reduced anxiety and/or in the presence of anxiolytic drugs may help to parse these effects.…”

Section: Discussionmentioning

confidence: 99%

Genetically Epilepsy-Prone Rats Display Anxiety-Like Behaviors and Neuropsychiatric Comorbidities of Epilepsy

et al. 2018

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Epilepsy is associated with a variety of neuropsychiatric comorbidities, including both anxiety and depression. Despite high occurrences of depression and anxiety seen in human epilepsy populations, little is known about the etiology of these comorbidities. Experimental models of epilepsy provide a platform to disentangle the contribution of acute seizures, genetic predisposition, and underlying circuit pathologies to anxious and depressive phenotypes. Most studies to date have focused on comorbidities in acquired epilepsies; genetic models, however, allow for the assessment of affective phenotypes that occur prior to onset of recurrent seizures. Here, we tested male and female genetically epilepsy-prone rats (GEPR-3s) and Sprague-Dawley controls in a battery of tests sensitive to anxiety-like and depressive-like phenotypes. GEPR-3s showed increased anxiety-like behavior in the open field test, elevated plus maze, light-dark transition test, and looming threat test. Moreover, GEPR-3s showed impaired prepulse inhibition of the acoustic startle reflex, decreased sucrose preference index, and impaired novel object recognition memory. We also characterized defense behaviors in response to stimulation thresholds of deep and intermediate layers of the superior colliculus (DLSC), but found no difference between strains. In sum, GEPR-3s showed inherited anxiety, an effect that did not differ significantly between sexes. The anxiety phenotype in adult GEPR-3s suggests strong genetic influences that may underlie both the seizure disorder and the comorbidities seen in epilepsy.

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“…To simulate the HPA dysregulation seen in the genetic and stress-based models of depression, researchers have used exogeneous corticosterone administration in rodents (160). Robust and highly reproducible anxiety-and depression-like behaviors have been reported following chronic oral administration of corticosterone, which may or may not lead to an elevation in the level of serum corticosterone (133,(161)(162)(163)(164)(165)(166)(167)(168)(169). In addition to the behavioral changes, chronic exogeneous corticosterone is associated with several neurobiological changes seen in MDD models including the disruption of adult hippocampal neurogenesis (170), and decreased hippocampal brain derived neurotrophic factor (BDNF) (171).…”

Section: Modelling Depression Using Exogeneous Corticosterone Adminismentioning

confidence: 99%

Cortisol and Major Depressive Disorder—Translating Findings From Humans to Animal Models and Back

Nandam¹,

Brazel²,

Zhou³

et al. 2020

Front. Psychiatry

154

103

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Major depressive disorder (MDD) is a global problem for which current pharmacotherapies are not completely effective. Hypothalamic-pituitary-adrenal (HPA) axis dysfunction has long been associated with MDD; however, the value of assessing cortisol as a biological benchmark of the pathophysiology or treatment of MDD is still debated. In this review, we critically evaluate the relationship between HPA axis dysfunction and cortisol level in relation to MDD subtype, stress, gender and treatment regime, as well as in rodent models. We find that an elevated cortisol response to stress is associated with acute and severe, but not mild or atypical, forms of MDD. Furthermore, the increased incidence of MDD in females is associated with greater cortisol response variability rather than higher baseline levels of cortisol. Despite almost all current MDD treatments influencing cortisol levels, we could find no convincing relationship between cortisol level and therapeutic response in either a clinical or preclinical setting. Thus, we argue that the absolute level of cortisol is unreliable for predicting the efficacy of antidepressant treatment. We propose that future preclinical models should reliably produce exaggerated HPA axis responses to acute or chronic stress a priori, which may, or may not, alter baseline cortisol levels, while also modelling the core symptoms of MDD that can be targeted for reversal. Combining genetic and environmental risk factors in such a model, together with the interrogation of the resultant molecular, cellular, and behavioral changes, promises a new mechanistic understanding of MDD and focused therapeutic strategies.

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Differential Peripheral Proteomic Biosignature of Fluoxetine Response in a Mouse Model of Anxiety/Depression

Cited by 27 publications

References 59 publications

Seeking for potential pathogenic genes of major depressive disorder in the Gene Expression Omnibus database

Seeking for potential pathogenic genes of major depressive disorder in the Gene Expression Omnibus database

Genetically Epilepsy-Prone Rats Display Anxiety-Like Behaviors and Neuropsychiatric Comorbidities of Epilepsy

Cortisol and Major Depressive Disorder—Translating Findings From Humans to Animal Models and Back

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