Elevated somatostatin interneuron long-term potentiation minimally regulates temporoammonic plasticity in a mouse model of Fragile X Syndrome
These data show that while SST-IN function is impaired in <i>Fmr1</i> <sup>-/y</sup> mice, circuit level plasticity is maintained. This study provides new insights into the function of drugs proposed for the treatment of Fragile X Syndrome.
Authors
- Emre Berk (ORCID: https://orcid.org/0000-0001-9674-5194)
- Max A Wilson (ORCID: https://orcid.org/0000-0003-3317-9433)
- Sam A. Booker (ORCID: https://orcid.org/0000-0003-1980-9873)
- Anna Sumera (ORCID: https://orcid.org/0000-0002-0058-4507)
Institutions
- Simons Foundation (US)
- University of Edinburgh (GB)
Publication Details
- Journal
- Frontiers in Pharmacology
- Published
- 2026-01-15
- DOI
- https://doi.org/10.3389/fphar.2025.1640921
- Primary Topic
- Genetics and Neurodevelopmental Disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Simons Initiative for the Developing Brain
- Medical Research Council