Reduced enteric Bdnf expression and TrkB-dependent regulation of Vip in a Mecp2-null mouse model of Rett syndrome-associated gastrointestinal dysmotility

In the Mecp2null mouse model of Rett syndrome-associated GI dysmotility, enteric Bdnf isoforms IV, VI, and II are markedly reduced while Vip expression is significantly decreased.

• Why it matters: GI dysmotility is common in Rett syndrome, but the molecular pathways in enteric circuits that drive impaired motility are not well defined.
• What they did: The study assessed MeCP2 expression in myenteric ganglia, measured Bdnf/TrkB and Vip/Vipr gene expression in dysmotile Mecp2null mice, and used conditional TrkB.FL loss plus integration with enteric single-cell/nucleus datasets and targeted qRTPCR.
• The result: TrkB.FL and TrkB.T1 were not significantly altered, Vipr1 and Vipr2 increased, and TrkB.FL loss reduced Vip without fully reproducing the Mecp2null VIPergic phenotype, implying BDNF–TrkB signaling contributes but is not sufficient.

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