SHUN-FA YANG2026-10-162026-10-162009-07-15Pure ID: 15369921Pure UUID: 471ac2dd-e099-4fef-9623-5957c938cd4710.1016/j.cbi.2009.03.013https://www.scopus.com/pages/publications/67349085489https://scholars.csmu.edu.tw/handle/123456789/30031Amphetamine (AMPH), a psychostimulant, is an appetite suppressant and may be regarded as a neurotoxin. It was reported that superoxide dismutase (SOD) and neuropeptide Y (NPY) participated in AMPH-mediated behavior response. However, molecular mechanisms underlying this action are not well known. Using feeding behavior as an indicator, this study investigated if protein kinase C (PKC)-δ signaling was involved. Rats were given daily with AMPH for 4 days. Changes in hypothalamic NPY, PKCδ and SOD mRNA contents were measured and compared. Results showed that the up-regulations of PKCδ and SOD mRNA levels following AMPH treatment were concomitant with the down-regulation of NPY mRNA level and the decrease of feeding. To further determine if PKCδ was involved, intracerebroventricular infusions of PKCδ antisense oligonucleotide were performed at 1 h before daily AMPH treatment in freely moving rats, and results showed that PKCδ knock-down could block the anorectic response and restore partially both NPY and SOD mRNA levels in AMPH-treated rats. It is suggested that central PKCδ signaling may play a functional role in the regulation of AMPH-mediated appetite suppression via a modification of hypothalamic NPY gene expression. Moreover, the increase of SOD during AMPH treatment may favor this modification.9enjournal article