Neuron, Journal Year: 2025, Volume and Issue: 113(7), P. 965 - 968
Published: April 1, 2025
Language: Английский
Neuron, Journal Year: 2025, Volume and Issue: 113(7), P. 965 - 968
Published: April 1, 2025
Language: Английский
National Journal of Clinical Anatomy, Journal Year: 2025, Volume and Issue: 14(1), P. 1 - 3
Published: Jan. 1, 2025
Language: Английский
Citations
0Frontiers in Neuroscience, Journal Year: 2025, Volume and Issue: 19
Published: April 17, 2025
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 genetic model of ASD, identify potential alterations the GI tract that could underlie ASD-associated comorbidities. enteric nervous system was characterized using Hematoxylin Eosin staining immunohistochemistry. permeability measured FITC-Dextran paracellular assay. Whole-GI motility time vivo carmine dye Colonic contractions were by tracking an ex Homozygous knock-out (KO) Shank3B-/- mice exhibit significantly altered epithelial increased permeability. An myenteric plexus density higher number HuC/D-expressing neurons ganglia observed colon mice. These slowed whole-GI transit reduced velocity propagation length colonic contractions. Compared heterozygous Shank3B+/- milder epithelial, neuronal, functional alterations. function, while partial phenotype. results indicate Shank3, whose mutation associated critical for its may contribute
Language: Английский
Citations
0Neuron, Journal Year: 2025, Volume and Issue: 113(7), P. 965 - 968
Published: April 1, 2025
Language: Английский
Citations
0