Transcriptional involvement of protein kinase C-alpha isozyme in amphetamine-mediated appetite suppression

  1. Yih-Shou Hsieh1,
  2. Shun-Fa Yang1,
  3. Hui-Ling Chiou2,
  4. Dong-Yih Kuo3

Article first published online: 3 AUG 2005

DOI: 10.1111/j.1460-9568.2005.04245.x

Issue

European Journal of Neuroscience

European Journal of Neuroscience

Volume 22, Issue 3, pages 715–723, August 2005

Additional Information

How to Cite

Hsieh, Y.-S., Yang, S.-F., Chiou, H.-L. and Kuo, D.-Y. (2005), Transcriptional involvement of protein kinase C-alpha isozyme in amphetamine-mediated appetite suppression. European Journal of Neuroscience, 22: 715–723. doi: 10.1111/j.1460-9568.2005.04245.x

Author Information

  1. 1

    Institute of Biochemistry, Chung Shan Medical University, Taichung, Taiwan, R.O.C.

  2. 2

    School of Medical Technology, Chung Shan Medical University, Taichung, Taiwan, R.O.C.

  3. 3

    Department of Physiology, Chung Shan Medical University, Taichung City 40201, Taiwan, R.O.C.

*Dr Dong-Yih Kuo, as above E-mail: dykuo@csmu.edu.tw

Publication History

  1. Issue published online: 11 AUG 2005
  2. Article first published online: 3 AUG 2005
  3. Received 21 March 2005, revised 6 May 2005, accepted 23 May 2005

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Keywords:

  • dopamine agonist;
  • feeding;
  • neuropeptide Y;
  • signal transduction

Abstract

Amphetamine (AMPH) is known as an anorectic agent. The anorectic action of AMPH has been attributed to its inhibitory action on hypothalamic neuropeptide Y (NPY), an appetite stimulant in the brain. The molecular mechanisms behind this anorectic action of AMPH are still unclear. This study investigated the possible role of protein kinase C (PKC) isotypes in this anorectic action. Results revealed that most PKC isotypes (α, βII, γ, δ, η, λ and ζ), except βI and ε isotypes, were stimulated during a repeated treatment of AMPH. Among these stimulated isotypes, three isotypes (α, δ, λ) were activated and expressed in a similar manner, while the other isotypes were expressed differently and specifically. To determine if PKCα was involved in the anorectic response of AMPH, the infusions of antisense oligonucleotide into the brain were performed 1 h before daily AMPH treatment in freely moving rats, and the results showed that PKCα knock down could block the anorectic response and restore NPY mRNA levels in AMPH-treated rats. These results suggest that PKC isotypes- (at least the α isotype), related modification of NPY gene expression in hypothalamus might play an essential role in the central regulation of AMPH-mediated feeding suppression.

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