{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T20:00:04Z","timestamp":1768593604721,"version":"3.49.0"},"reference-count":70,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2024,11,29]],"date-time":"2024-11-29T00:00:00Z","timestamp":1732838400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>The regulatory neuropeptide Y (NPY) is implicated in anxiety and post-traumatic stress disorder (PTSD)-related behaviors. NPY exerts its effects through 5 receptor subtypes, with Y1 and Y2 receptors being predominantly expressed in the rat brain. Activation of Y1 by full-length NPY1-36 induces anxiolytic effects, whereas Y2 binds truncated peptides, eliciting region-specific anxiogenic responses. Dipeptidyl peptidase-IV (DPP-IV) cleaves NPY, thereby modulating its functionality. Sitagliptin, a DPP-IV inhibitor (DPP-IV-I), inhibits the degradation of various vasoactive peptides, including cerebral NPY. As such, the therapeutic potential of DPP-IV-I following a traumatic event remains inconclusive. We assessed the effects of a highly selective DPP-IV-I, administered either shortly after the stressor or intermittently over 3 days, on behavioral outcomes using the predator scent stress (PSS) model of PTSD.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Rats exposed to PSS or sham-PSS received a single dose of sitagliptin (10 or 30\u00a0mg\/kg) or saline 1 hour post-exposure, or repeated doses over 3 days (20\u00a0mg\/kg). Behavioral outcomes were evaluated using the elevated plus maze and acoustic startle response at 7 days post-exposure. Additionally, rats exposed to PSS or sham-PSS were treated with sitagliptin (30\u00a0mg\/kg) or saline, and their brains were prepared for immunofluorescence and enzyme-linked immunosorbent assay (ELISA).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Sitagliptin did not attenuate anxiety-related behaviors or PTSD-related behavior prevalence compared to saline. Notably, the 30\u00a0mg\/kg dose increased NPY levels in several brain regions without affecting NPY-Y1 levels.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>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.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ijnp\/pyae062","type":"journal-article","created":{"date-parts":[[2024,12,3]],"date-time":"2024-12-03T19:03:28Z","timestamp":1733252608000},"source":"Crossref","is-referenced-by-count":11,"title":["Exploring the Anxiolytic Potential of NPY by a Dipeptidyl Peptidase-IV Inhibitor in an Animal Model of PTSD"],"prefix":"10.1093","volume":"27","author":[{"given":"Matan","family":"Dahan","sequence":"first","affiliation":[{"name":"Anxiety and Stress Research Unit, Ministry of Health, Beer-Sheva Mental Health Center , Beer-Sheva ,","place":["Israel"]},{"name":"Department of Psychology, Ben-Gurion University of the Negev , Beer-Sheva ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joseph","family":"Zohar","sequence":"additional","affiliation":[{"name":"Post-Trauma Center, Sheba Medical Center, Tel Aviv University , Tel Aviv ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Doron","family":"Todder","sequence":"additional","affiliation":[{"name":"Faculty of Health Sciences, Ben-Gurion University of the Negev , Beer-Sheva ,","place":["Israel"]},{"name":"Anxiety and Stress Research Unit, Ministry of Health, Beer-Sheva Mental Health Center , Beer-Sheva ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6946-532X","authenticated-orcid":false,"given":"Aleksander A","family":"Math\u00e9","sequence":"additional","affiliation":[{"name":"Karolinska Institute Clinical Neuroscience, Karolinska University Hospital Huddinge , Stockholm ,","place":["Sweden"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4762-1969","authenticated-orcid":false,"given":"Hagit","family":"Cohen","sequence":"additional","affiliation":[{"name":"Faculty of Health Sciences, Ben-Gurion University of the Negev , Beer-Sheva ,","place":["Israel"]},{"name":"Anxiety and Stress Research Unit, Ministry of Health, Beer-Sheva Mental Health Center , Beer-Sheva ,","place":["Israel"]},{"name":"Department of Psychology, Ben-Gurion University of the Negev , Beer-Sheva ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2024,11,29]]},"reference":[{"key":"2024121808561072800_CIT0001","doi-asserted-by":"crossref","first-page":"584","DOI":"10.1038\/306584a0","article-title":"Neuropeptide Y distribution in human 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