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Loss of enteric BDNF–TrkB signaling and VIPergic dysfunction underlie gastrointestinal dysmotility in a Mecp2-null mouse model of Rett syndrome

2026-04-15

Abstract excerpt

Gastrointestinal (GI) dysmotility is a highly prevalent and clinically significant feature of Rett syndrome (RTT), yet its underlying mechanisms remain poorly defined. Here, we investigated these mechanisms of GI dysmotility in a Mecp2-null mouse model of RTT. First, we observed that MeCP2 was expressed in murine myenteric ganglia, including in enteric neurons and that Mecp2-null males developed maturation-assoc...

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Literature Corpus work: a8b18396-ebd1-5cfe-9540-490d3a0a7ddb
DOI: 10.64898/2026.04.12.718037

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Loss of enteric BDNF–TrkB signaling and VIPergic dysfunction underlie gastrointestinal dysmotility in a Mecp2-null mouse model of Rett syndromeDOI 10.64898/2026.04.12.718037Read

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Loss of enteric BDNF–TrkB signaling and VIPergic dysfunction underlie gastrointestinal dysmotility in a <i>Mecp2-null</i> mouse model of Rett syndrome

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