<i>Shank3</i> mutation manifests in abnormal gastrointestinal morphology and function in mice.

ABSTRACT:

Background

Gastrointestinal (GI) comorbidities are common among those with Autism Spectrum Disorder (ASD), but their etiology is not well understood. This study aimed to characterize gastrointestinal morphology and function in Shank3B mutant mice, a common genetic model of ASD, to identify potential alterations to the GI tract that could underlie ASD-associated GI comorbidities.

Methods

GI and enteric nervous system morphology was characterized using Hematoxylin and Eosin staining and immunohistochemistry. GI permeability was measured using the FITC-Dextran paracellular permeability assay. Whole-GI tract motility time was measured in vivo using the carmine dye motility assay. Colonic contractions were characterized by tracking motility using an ex vivo motility

SUBMITTER: Eberly GL 

PROVIDER: S-EPMC12043642 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature