期刊
FRONTIERS IN NEUROSCIENCE
卷 17, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fnins.2023.1287057
关键词
autism spectrum disorder; gastrointestinal dysmotility; Cntnap2; Caspr2; enteric nervous system; sensory neurons; intrinsic primary afferent neurons
This study investigates the role of Cntnap2 in gastrointestinal (GI) function by examining its expression in the enteric nervous system (ENS) and assessing GI motility in mutant mice. The results suggest that Cntnap2 plays a role in GI function and may serve as a molecular link between autism spectrum disorder (ASD) and GI dysfunction.
Gastrointestinal (GI) symptoms are highly prevalent among individuals with autism spectrum disorder (ASD), but the molecular link between ASD and GI dysfunction remains poorly understood. The enteric nervous system (ENS) is critical for normal GI motility and has been shown to be altered in mouse models of ASD and other neurological disorders. Contactin-associated protein-like 2 (Cntnap2) is an ASD-related synaptic cell-adhesion molecule important for sensory processing. In this study, we examine the role of Cntnap2 in GI motility by characterizing Cntnap2's expression in the ENS and assessing GI function in Cntnap2 mutant mice. We find Cntnap2 expression predominately in enteric sensory neurons. We further assess in vivo and ex vivo GI motility in Cntnap2 mutants and show altered transit time and colonic motility patterns. The overall organization of the ENS appears undisturbed. Our results suggest that Cntnap2 plays a role in GI function and may provide a molecular link between ASD and GI dysfunction.
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