Loss of enteric BDNF–TrkB signaling and VIPergic dysfunction underlie gastrointestinal dysmotility in a <i>Mecp2-null</i> mouse model of Rett syndrome
VIPergic phenotype, indicating that impaired BDNF-TrkB signaling contributes to, but does not completely explain, the GI dysmotility in this model of RTT. Together, these findings identify enteric BDNF-TrkB and VIPergic dysfunction as key mechanisms underlying GI dysmotility in RTT.
Authors
- Jared Slosberg (ORCID: https://orcid.org/0000-0002-1803-2815)
- Michela Fagiolini (ORCID: https://orcid.org/0000-0003-2807-803X)
- Xavier Valencia
- Subhash Kulkarni (ORCID: https://orcid.org/0000-0002-2298-0623)
- Alan Consorti (ORCID: https://orcid.org/0000-0002-4586-8239)
- Srinivas N. Puttapaka
- Mahalakshmi Rajkumar
- Su Min Hong (ORCID: https://orcid.org/0009-0006-8472-9924)
- Philippa Seika
- Israel Abebe Admasu
- Gamze Sonmez
- Ainsleigh Scott
Institutions
- Boston Children's Hospital (US)
- Beth Israel Deaconess Medical Center (US)
- Harvard University (US)
- Johns Hopkins University (US)
- Johns Hopkins Medicine (US)
Publication Details
- Journal
- bioRxiv (Cold Spring Harbor Laboratory)
- Published
- 2026-04-15
- DOI
- https://doi.org/10.64898/2026.04.12.718037
- Primary Topic
- Genetics and Neurodevelopmental Disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Burroughs Wellcome Fund