Functional imaging shows how intestinal and liverdiseases mutually influence each other NatureComms
mice were sacrificed for further analysis due to low reproductive potential and early spontaneous death.To explore whether TNFα was the mediator to induce DSS-triggered inhibition of bile acid metabolism, littermates of 8–10-week-oldmice were injected with 10 mg/kg infliximab or PBS daily for 3 consecutive days. At day 9, mice were sacrificed for analysis. Fresh DSS solution was replaced every second day, and body weight was recorded every day.
To perform Sirius red staining, rehydrated sections were immersed in 0.1% Sirius red solution for 1 h. The samples were then incubated twice in 0.5% glacial acetic acid for 15 s each. Lastly, the tissue sections were dehydrated in the same way as for H&E staining. Images were obtained with AxioVision 4.9 and positive areas of Sirius red staining were quantified by ImageJ .H&E-stained colonic sections were evaluated by a pathologist as previously described.
Regarding the co-staining of HNF4α and phosphorylated P65 , the slides were incubated with the antibody mixture overnight at 4 °C. After washing with PBST, liver sections were serially incubated with donkey anti-goat IgG Alexa 647 and goat anti-rabbit IgG Alexa 488 for 1 hour at RT. Other steps were the same as for HNF4α and TUNEL co-staining.
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Alcohol-induced damage to the fimbria/fornix reduces hippocampal-prefrontal cortex connection during early abstinence - Acta Neuropathologica CommunicationsIntroduction Alcohol dependence is characterized by a gradual reduction in cognitive control and inflexibility to contingency changes. The neuroadaptations underlying this aberrant behavior are poorly understood. Using an animal model of alcohol use disorders (AUD) and complementing diffusion-weighted (dw)-MRI with quantitative immunohistochemistry and electrophysiological recordings, we provide causal evidence that chronic intermittent alcohol exposure affects the microstructural integrity of the fimbria/fornix, decreasing myelin basic protein content, and reducing the effective communication from the hippocampus (HC) to the prefrontal cortex (PFC). Using a simple quantitative neural network model, we show how disturbed HC-PFC communication may impede the extinction of maladaptive memories, decreasing flexibility. Finally, combining dw-MRI and psychometric data in AUD patients, we discovered an association between the magnitude of microstructural alteration in the fimbria/fornix and the reduction in cognitive flexibility. Overall, these findings highlight the vulnerability of the fimbria/fornix microstructure in AUD and its potential contribution to alcohol pathophysiology. Summary Fimbria vulnerability to alcohol underlies hippocampal-prefrontal cortex dysfunction and correlates with cognitive impairment.
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