Happy gut, happy mouse? Following is an article cited from the journal Cell that talks about experiments with probiotics. You can find primary articles in the database below, specifically Pubmed or Pubmed Central. Primary articles are those that describe original research done by the author as described on this page. Review or lay articles are recaps of other scientists' research. If the article you want does not come back from Iinterlibrary Loan as filled, please come see any research librarian and we will get it for you.
The MIA model recapitulates GI comorbidities linked to a subset of ASD individuals
Targeting the microbiota treats specific GI and behavioral symptoms
Neurodevelopmental disorders, including autism spectrum disorder (ASD), are defined by core behavioral impairments; however, subsets of individuals display a spectrum of gastrointestinal (GI) abnormalities. We demonstrate GI barrier defects and microbiota alterations in the maternal immune activation (MIA) mouse model that is known to display features of ASD. Oral treatment of MIA offspring with the human commensal Bacteroides fragilis corrects gut permeability, alters microbial composition, and ameliorates defects in communicative, stereotypic, anxiety-like and sensorimotor behaviors. MIA offspring display an altered serum metabolomic profile, and B. fragilis modulates levels of several metabolites. Treating naive mice with a metabolite that is increased by MIA and restored by B. fragilis causes certain behavioral abnormalities, suggesting that gut bacterial effects on the host metabolome impact behavior. Taken together, these findings support a gut-microbiome-brain connection in a mouse model of ASD and identify a potential probiotic therapy for GI and particular behavioral symptoms in human neurodevelopmental disorders.
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