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    Lots of interesting goodies in this one, @carlsonbjj!

    A synopsis of some of the more salient points for you, @rhonda

    The microbiome affecting the blood-brain barrier:

    Exposure of GF adult mice to the fecal microbiota from pathogen-free donors decreased BBB permeability and increased the expression of tight junction proteins (Braniste et al., 2014). Moreover, monocolonization of the intestine of GF adult mice with short chain fatty acid (SCFA)-producing bacterial strains normalized BBB permeability whilst sodium butyrate was associated with increased expression of occludin in the frontal cortex and hippocampus (Braniste et al., 2014). This study strengthens the hypothesis that the BBB may also be vulnerable to changes in the gut microbiota. […]

    Disrupted microbiome affecting susceptibility to stress in adulthood and altering the development of the HPA axis:

    It is plausible that subtle alterations in microbiota acquisition or maintenance in early life may act as a vulnerability factor, impacting on (neuro)endocrine and (neuro)immune signaling pathways of the brain-gut-microbiota axis, disruption of which may subsequently predispose to stress-related disorders in adulthood (Borre et al., 2014). Notably, animals devoid of a microbiota exhibit reduced levels of anxiety but an exaggerated neuroendocrine response to stress (Sudo et al., 2004). The most pronounced impacts of the microbiota may occur early in life during critical neurodevelopmental phases (Borre et al., 2014). It is evident that the gut microbiota is required for the normal development of the hypothalamic pituitary adrenal (HPA) axis and that there is a certain period in early life when colonization must occur to ensure normal development of this critical stress signaling pathway (Sudo et al., 2004; Moloney et al., 2014).

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      Although GF mouse model isn’t a great correlate for real life.