PEI-NI CHEN2026-10-162026-10-162012-03-01Pure ID: 15212954Pure UUID: b93db074-474a-4c2b-b4c0-5dba8fd5e9b010.1016/j.neuropharm.2011.11.014https://www.scopus.com/pages/publications/84856451043https://scholars.csmu.edu.tw/handle/123456789/30011This study determined if transcription factor NF-κB is involved in the effect of amphetamine (AMPH)-mediated feeding response. Moreover, possible roles of hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) were also investigated. AMPH was administered daily to rats for four days. Changes in NF-κB, NPY and POMC expression were assessed and compared. The NPY gene was down-regulated with maximal response on Day 2 during AMPH treatment, which was consistent with the response to feeding behavior. In contrast, NF-κB and POMC genes were up-regulated, and their expression was increased by about 200% and 450%, respectively, with maximal response on Day 2. Moreover, NF-κB DNA binding ability and expression were increased similar to that of POMC. To examine further if NF-κB was involved, intracerebroventricular infusion of NF-κB antisense oligonucleotide was performed 1 h before the daily AMPH dosing in freely moving rats. Results showed that NF-κB knockdown could modify AMPH anorexia as well as NPY and POMC expression. The present findings prove that cerebral NF-κB participates in AMPH-mediated appetite suppression, possibly by modulating NPY and POMC expression. These results may aid in therapeutic research on AMPH and AMPH-like anti-obesity drugs.11enjournal article