Exploring the Anxiolytic Potential of NPY by a Dipeptidyl Peptidase-IV Inhibitor in an Animal Model of PTSD
The findings suggest that sitagliptin-induced upregulation of NPY levels shortly after PSS is insufficient to prevent the development of post-traumatic responses. The effectiveness of NPY signaling may be influenced by factors beyond peptide concentration alone, potentially limiting its therapeutic efficacy. Activation of NPY-Y1 receptors, rather than merely increasing NPY levels, appears to be crucial for modulating anti-anxiety and post-traumatic responses.
Authors
- Joseph Zohar (ORCID: https://orcid.org/0000-0002-6925-9104)
- Hagit Cohen (ORCID: https://orcid.org/0000-0002-4762-1969)
- Aleksander A. Mathé (ORCID: https://orcid.org/0000-0002-6946-532X)
- M Dahan (ORCID: https://orcid.org/0000-0002-6734-8699)
- Todder Doron
Institutions
- Ben-Gurion University of the Negev (IL)
- Karolinska University Hospital (SE)
- Tel Aviv University (IL)
- Sheba Medical Center (IL)
- Karolinska Institutet (SE)
- The Technological College of Beer Sheva (IL)
- Ministry of Health of the Russian Federation (RU)
Publication Details
- Journal
- The International Journal of Neuropsychopharmacology
- Published
- 2024-11-29
- DOI
- https://doi.org/10.1093/ijnp/pyae062
- Citations
- 11
- Primary Topic
- Neuropeptides and Animal Physiology
- Type
- article
- Field-Weighted Citation Impact
- 2.95