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To further determine if PKA was involved, intracerebroventricular infusions of antisense oligodeoxynucleotide were performed at 60 min before daily PPA treatment in freely moving rats. Results showed that daily PKA, CREB, and POMC expression were increased following PPA treatment, which showed a closely reverse relationship with alterations of decreased feeding behaviors and NPY mRNA levels. Results also showed that PKA knock-down could block PPA-induced anorexia as well as restore NPY mRNA level, indicating the involvement of PKA signaling in the regulation of NPY gene expression. It is suggested that hypothalamic PKA signaling may participate in the central regulation of PPA-mediated appetite suppression via the modulation of hypothalamic NPY gene expression. The present findings reveal that manipulations at the molecular level of PKA or cAMP may allow the development of therapeutic agents to improve the undesirable properties of PPA or other amphetamine-like anorectic drugs.<\/jats:p>","DOI":"10.1152\/physiolgenomics.00110.2007","type":"journal-article","created":{"date-parts":[[2007,8,8]],"date-time":"2007-08-08T01:44:32Z","timestamp":1186537472000},"page":"306-314","source":"Crossref","is-referenced-by-count":8,"title":["Transcript of protein kinase A knock-down modulates feeding behavior and neuropeptide Y gene expression in phenylpropanolamine-treated rats"],"prefix":"10.1152","volume":"31","author":[{"given":"Yih-Shou","family":"Hsieh","sequence":"first","affiliation":[{"name":"Institute of Biochemistry, Central Taiwan University of Science and Technology, Taichung City, Taiwan, Republic of 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