The Zonulin-transgenic mouse displays behavioral alterations ameliorated via depletion of the gut microbiota

Author(s):  
Alba Miranda-Ribera ◽  
Gloria Serena ◽  
Jundi Liu ◽  
Alessio Fasano ◽  
Marcy A. Kingsbury ◽  
...  
2018 ◽  
Vol 12 ◽  
Author(s):  
Sophie Leclercq ◽  
Tiphaine Le Roy ◽  
Laure Bindels ◽  
Caroline Quoilin ◽  
Audrey Neyrinck ◽  
...  

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 764
Author(s):  
Alisa Arslanova ◽  
Aksiniya Tarasova ◽  
Anastasia Alexandrova ◽  
Vera Novoselova ◽  
Ilnar Shaidullov ◽  
...  

Accumulating clinical and preclinical data indicate a prominent role of gut microbiota in regulation of physiological functions. The gut–brain axis imbalance due to gut dysbiosis is associated with a range of neurodegenerative diseases. Probiotics were suggested not only to restore intestinal dysbiosis but also modulate stress response and improve mood and anxiety symptoms. In this study, we assessed the effects of probiotic lactobacilli on behavioral reactions, the level of oxidative stress and microbiota content in mice administered to broad-spectrum antibiotics. Our study demonstrates that antibiotic treatment of adolescent mice for two weeks resulted in higher mortality and lower weight gain and induced significant changes in behavior including lower locomotor and exploratory activity, reduced muscle strength, visceral hypersensitivity, higher level of anxiety and impaired cognitive functions compared to the control group. These changes were accompanied by decreased diversity and total amount of bacteria, abundance of Proteobacteria and Verrucomicrobia phyla, and reduced Firmicutes/Bacteroides ratio in the gut microbiota. Moreover, a higher level of oxidative stress was found in brain and skeletal muscle tissues of mice treated with antibiotics. Oral administration of two Lactobacillus strains prevented the observed changes and improved not only microbiota content but also the behavioral alterations, suggesting a neuroprotective and antioxidant role of probiotics.


CNS Spectrums ◽  
2005 ◽  
Vol 10 (3) ◽  
pp. 207-222 ◽  
Author(s):  
Debby Van Dam ◽  
Ellen Vloeberghs ◽  
Dorothee Abramowski ◽  
Matthias Staufenbiel ◽  
Peter Paul De Deyn

AbstractAnimal models are considered essential in research ensuing elucidation of human disease processes and subsequently, testing of potential therapeutic strategies. This is especially true for neurodegenerative disorders, in which the first steps in pathogenesis are often not accessible in human patients. Alzheimer's disease is vastly becoming a major medical and socioeconomic problem in our aging society. Valid animal models for this uniquely human condition should exhibit histopathological, biochemical, cognitive, and behavioral alterations observed in Alzheimer's disease patients. Major progress has been made since the understanding of the genetic basis of Alzheimer's disease and the development and improvement of transgenic mouse models. All present Alzheimer's disease models developed are partial but nevertheless essential in further unraveling the nature and spatial and temporal development of the complex molecular pathology underlying this condition. One of the more recent transgenic attempts to mode Alzheimer's disease is the APP23 transgenic mouse. This article describes the development and assessment of this human amyloid precursor protein overexpression model. We summarize histopathological and biochemical, cognitive and behavioral observations made in heterozygous APP23 mice, thereby emphasizing the model's contribution to clarification of neurodegenerative disease mechanisms. In addition, the first therapeutic interventions in the APP23 model are included.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Grégoire Chevalier ◽  
Eleni Siopi ◽  
Laure Guenin-Macé ◽  
Maud Pascal ◽  
Thomas Laval ◽  
...  

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.


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