Intracerebroventricular knockdown of NPY1R disrupts NPY1R-GALR2/TrkB heteroreceptor complexes without affecting neuroplasticity or depressive-like behaviour
Transient ICV knockdown effectively disrupts NPY1R heteroreceptor complexes but fails to impact neurogenesis or depressive-like behaviour, indicating compensatory mechanisms that preserve hippocampal plasticity. Within the time window and conditions tested, transient NPY1R knockdown disrupted GALR2/TrkB heteroreceptor complexes without altering neurogenesis or depressive-like behaviour, delineating receptor-complex-level target engagement and motivating studies using sustained and circuit-specific manipulations to assess therapeutic potential.
Authors
- Jesús Romero-Imbroda (ORCID: https://orcid.org/0000-0002-0120-481X)
- Pedro Jesús Serrano-Castro (ORCID: https://orcid.org/0000-0002-3414-2707)
- Manuel Narváez (ORCID: https://orcid.org/0000-0003-0922-4900)
- Dasiel O. Borroto‐Escuela (ORCID: https://orcid.org/0000-0002-5736-373X)
- Amelia Díaz-Casares
- Kjell Fuxé (ORCID: https://orcid.org/0000-0001-8491-4288)
- Carlos Arrabal-Gómez
- Isabel Moreno-Madrid
Institutions
- Karolinska Institutet (SE)
- Hospital Regional Universitario de Málaga (ES)
- Andalusian Centre for Nanomedicine and Biotechnology (ES)
- Instituto de Investigación Biomédica de Málaga (ES)
- Universidad de Málaga (ES)
Publication Details
- Journal
- Journal of Psychopharmacology
- Published
- 2025-11-27
- DOI
- https://doi.org/10.1177/02698811251389528
- Primary Topic
- Neurogenesis and neuroplasticity mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00