scholarly journals Oral Probiotics Ameliorate the Behavioral Deficits Induced by Chronic Mild Stress in Mice via the Gut Microbiota-Inflammation Axis

2018 ◽  
Vol 12 ◽  
Author(s):  
Nannan Li ◽  
Qi Wang ◽  
Yan Wang ◽  
Anji Sun ◽  
Yiwei Lin ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Behavioral Deficits

scholarly journals The impact of gut microbiota on depressive-like behaviors and adult hippocampal neurogenesis requires the endocannabinoid system

2019 ◽  
Author(s):  
Grégoire Chevalier ◽  
Eleni Siopi ◽  
Laure Guenin-Macé ◽  
Maud Pascal ◽  
Thomas Laval ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Endocannabinoid System ◽  
Chronic Mild Stress ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Mild Stress ◽  
Microbiota Composition ◽  
The Impact

SUMMARYDepression is the leading cause of disability worldwide. Recent observations have revealed an association between mood disorders and alterations of the intestinal microbiota, but causality remains yet to be established. Here, using unpredictable chronic mild stress (UCMS) as a mouse model of depression, we show that the UCMS mice display phenotypic alterations — characterized by an altered gut microbiota composition, a reduced adult hippocampal neurogenesis and a depressive-like behaviors — which could be transferred from UCMS donors to naïve recipient mice by fecal microbiota transplantation. The cellular and behavioral alterations observed in recipient mice were accompanied by a decrease in the endocannabinoid (eCB) signaling due to lower peripheral levels of fatty acid precursors of eCB ligands. The adverse effects of UCMS-transferred microbiota on adult neurogenesis and behavior in naïve recipient mice were alleviated by selectively enhancing the central eCB tone or by adding arachidonic acid, a fatty acid precursor of eCB ligands, to the diet. In the gut of both UCMS donors and recipients, the microbiota composition was characterized by a relative decrease in Lactobacilli abundance, and complementation of the UCMS recipient microbiota with a strain of the Lactobacilli genus was sufficient to restore normal eCB brain levels, hippocampal neurogenesis and to alleviate depressive-like behaviors. Our findings provide a mechanistic scenario for how chronic stress, diet and gut microbiota dysbiosis generate a pathological feed-forward loop that contributes to despair behavior via the central eCB system.

scholarly journals Dapoxetine: An Innovative Approach in the Therapeutic Management In Animal Model of Depression

2016 ◽  
Vol 2 (1) ◽  
pp. 15
Author(s):  
Hira Rafi ◽  
Muhammad Farhan
Keyword(s):  
Learned Helplessness ◽  
Chronic Mild Stress ◽  
Repeated Administration ◽  
Mild Stress ◽  
Behavioral Deficits ◽  
Unpredictable Chronic Mild Stress ◽  
Field Environment ◽  
Novel Approach ◽  
Synaptic Receptors ◽  
Familiar Environment

Stress is a complicated condition that effects on person’s mental and physical health, and it is the precursor of other psychological disorders mainly depression. Serotonin (5-Hydroxytryptamine; 5-HT) is well known to have hypofunction in unpredictable chronic mild stress whereas, unpredictable chronic mild stress (UCMS) has produced the most steady and continuous results of anhedonia and learned helplessness particularly in rats. The stress-induced depressive like behavior can be reversed by many antidepressants such as SSRIs. Selective serotonin [5-hydroxytryptamine (5-HT)] reuptake inhibitors (SSRIs) is mostly prescribed antidepressant that can deplete neurochemical and behavioral deficits. The present study was designed to investigate whether repeated administration of dapoxetine at dose (1.0 mg/kg) could reverse the behavioral deficits induced by UCMS in rat model of depression. UCMS induced behavioral deficits. Locomotor  activity in familiar environment (home cage), novel (open field) environment and anxiolytic behavior in light/dark activity box were greater in unstressed group than stressed group. The inhibition of serotonin reuptake at pre-synaptic receptors by repeated dapoxetine administration is mainly the mechanism involved and discussed. This particular study may assist in novel approach for understanding the interaction between stress and behavioral functions and extending the therapeutic use of dapoxetine.

scholarly journals S112. EFFECT OF CHRONIC LURASIDONE TREATMENT ON CHRONIC MILD STRESS-INDUCED BEHAVIORAL DEFICITS: THE POTENTIAL ROLE FOR GLUCOCORTICOID RECEPTOR SIGNALING

2019 ◽  
Vol 45 (Supplement_2) ◽  
pp. S349-S350
Author(s):  
Francesca Calabrese ◽  
Paola Brivio ◽  
Giulia Sbrini ◽  
Monika Niemczyk ◽  
Magdalena Lason ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Potential Role ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Receptor Signaling ◽  
Behavioral Deficits

scholarly journals Prophylactic efficacy of riluzole against anxiety- and depressive-like behaviors in two rodent stress models

2020 ◽  
Author(s):  
Corey Fee ◽  
Keith A. Misquitta ◽  
Etienne Sibille ◽  
Robert M. Berman ◽  
Vladimir Coric ◽  
...  
Keyword(s):  
Traumatic Stress ◽  
Learned Helplessness ◽  
Prophylactic Treatment ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Post Traumatic Stress ◽  
Major Depressive ◽  
Behavioral Deficits ◽  
Unpredictable Chronic Mild Stress ◽  
Post Traumatic

AbstractBackgroundChronic stress-related illnesses, such as major depressive disorder (MDD) and post-traumatic stress disorder (PTSD), share symptomatology, including anxiety, anhedonia, and helplessness. Across disorders, neurotoxic dysregulated glutamate (Glu) signaling may underlie symptom emergence. Current first-line antidepressant drugs (ADs), which do not directly target Glu signaling, fail to provide adequate benefit for many patients and are associated with high relapse rates. Riluzole modulates glutamatergic neurotransmission by increasing metabolic cycling and modulating signal transduction. Clinical studies exploring riluzole’s efficacy in stress-related disorders have provided varied results. However, the utility of riluzole for treating specific symptom dimensions or as a prophylactic treatment has not been comprehensively assessed.MethodsWe investigated whether chronic prophylactic riluzole (∼12-15/kg/day p.o.) could prevent the emergence of behavioral deficits induced by unpredictable chronic mild stress (UCMS) in mice. We assessed i) anxiety-like behavior using the elevated-plus maze, open field test, and novelty-suppressed feeding, ii) mixed anxiety/anhedonia-like behavior in the novelty-induced hypophagia test and, iii) anhedonia-like behavior using the sucrose consumption test. Z-scoring summarized changes across tests measuring similar outcomes. In a separate learned helplessness (LH) cohort, we investigated whether chronic preventative riluzole treatment could block the development of helplessness-like behavior.ResultsUCMS induced an elevation in anxiety-, anhedonia-like behavior, and overall behavioral emotionality that was blocked by prophylactic riluzole. In the LH cohort, preventative riluzole blocked the development of helplessness-like behavior.ConclusionThis study supports the utility of riluzole as a prophylactic medication, and potential relapse-preventing treatment targeting anhedonia, anxiety, and helplessness symptoms associated with stress-related disorders.Significance StatementRiluzole is a glutamate-modulating drug with mixed evidence of efficacy in clinical studies of patients with stress-related disorders. Based on evidence suggesting that glutamatergic dysfunction contributes to the pathogenesis of stress-related disorders, we investigated whether prophylactic treatment with riluzole could prevent the onset of behavioral deficits induced by unpredictable chronic mild stress or learned helplessness in mice. Riluzole effectively prevented the emergence of anxiety-, anhedonia-like behavior, and overall behavioral emotionality in mice exposed to unpredictable chronic mild stress. In a separate cohort, riluzole blocked the emergence of helplessness-like behavior as measured in an active avoidance paradigm. These results support testing riluzole as a prophylactic treatment strategy in stress-related illnesses such as major depressive disorder or post-traumatic stress disorder.

scholarly journals Effect of gut microbiota on depressive-like behaviors in mice is mediated by the endocannabinoid system

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Grégoire Chevalier ◽  
Eleni Siopi ◽  
Laure Guenin-Macé ◽  
Maud Pascal ◽  
Thomas Laval ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Adverse Effects ◽  
Mouse Model ◽  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Endocannabinoid System ◽  
Chronic Mild Stress ◽  
Fecal Microbiota ◽  
Mild Stress ◽  
Behavioral Alterations

AbstractDepression is the leading cause of disability worldwide. Recent observations have revealed an association between mood disorders and alterations of the intestinal microbiota. Here, using unpredictable chronic mild stress (UCMS) as a mouse model of depression, we show that UCMS mice display phenotypic alterations, which could be transferred from UCMS donors to naïve recipient mice by fecal microbiota transplantation. The cellular and behavioral alterations observed in recipient mice were accompanied by a decrease in the endocannabinoid (eCB) signaling due to lower peripheral levels of fatty acid precursors of eCB ligands. The adverse effects of UCMS-transferred microbiota were alleviated by selectively enhancing the central eCB or by complementation with a strain of the Lactobacilli genus. Our findings provide a mechanistic scenario for how chronic stress, diet and gut microbiota generate a pathological feed-forward loop that contributes to despair behavior via the central eCB system.

Sodium Butyrate Functions as an Antidepressant and Improves Cognition with Enhanced Neurotrophic Expression in Models of Maternal Deprivation and Chronic Mild Stress

2014 ◽  
Vol 11 (4) ◽  
pp. 359-366 ◽  
Author(s):  
Samira Valvassori ◽  
Roger Varela ◽  
Camila Arent ◽  
Gustavo Dal-Pont ◽  
Tamara Bobsin ◽  
...  
Keyword(s):  
Sodium Butyrate ◽  
Chronic Mild Stress ◽  
Maternal Deprivation ◽  
Mild Stress
Sign in / Sign up

Export Citation Format

Share Document