The neuropeptide Y Y1 receptor knockdown modulates activator protein 1-involved feeding behavior in amphetamine-treated rats

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• 作者：Yih-Shou Hsieh (1)
  Pei-Ni Chen (1)
  Ching-Han Yu (2)
  Jiuan-Miaw Liao (2)
  Dong-Yih Kuo (2)
  
• 关键词：NPY ; Y1 receptor ; c ; Fos ; c ; Jun ; AP ; 1 ; Appetite ; Hypothalamus
• 刊名：Molecular Brain
• 出版年：2013
• 出版时间：December 2013
• 年：2013
• 卷：6
• 期：1
• 全文大小：361 KB
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• 作者单位：Yih-Shou Hsieh (1)
  Pei-Ni Chen (1)
  Ching-Han Yu (2)
  Jiuan-Miaw Liao (2)
  Dong-Yih Kuo (2)
  
  1. Institute of Biochemistry and Biotechnology, Chung Shan Medical University and Chung Shan Medical University Hospital, Taichung City, 40201, Taiwan
  2. Department of Physiology, Chung Shan Medical University and Chung Shan Medical University Hospital, Taichung City, 40201, Taiwan
  
• ISSN：1756-6606

文摘

Background Hypothalamic neuropeptide Y (NPY) and two immediate early genes, c-fos and c-jun, have been found to be involved in regulating the appetite-suppressing effect of amphetamine (AMPH). The present study investigated whether cerebral catecholamine (CA) might regulate NPY and POMC expression and whether NPY Y1 receptor (Y1R) participated in activator protein-1 (AP-1)–mediated feeding. Methods Rats were given AMPH daily for 4?days. Changes in the expression of NPY, Y1R, c-Fos, c-Jun, and AP-1 were assessed and compared. Results Decreased CA could modulate NPY and melanocortin receptor 4 (MC4R) expressions. NPY and food intake decreased the most on Day 2, but Y1R, c-Fos, and c-Jun increased by approximately 350%, 280%, and 300%, respectively, on Day 2. Similarly, AP-1/DNA binding activity was increased by about 180% on Day 2. The expression patterns in Y1R, c-Fos, c-Jun, and AP-1/DNA binding were opposite to those in NPY during AMPH treatment. Y1R knockdown was found to modulate the opposite regulation between NPY and AP-1, revealing an involvement of Y1R in regulating NPY/AP-1–mediated feeding. Conclusions These results point to a molecular mechanism of CA/NPY/Y1R/AP-1 signaling in the control of AMPH-mediated anorexia and may advance the medical research of anorectic and anti-obesity drugs.