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

doi:10.1186/1756-6606-6-46

CSMUIR > Medical College > The Institute of Biochemistry, Microbiology and Immunology > Journal Paper > Item 310902500/11433

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11433

Title:	The neuropeptide Y Y1 receptor knockdown modulates activator protein 1-involved feeding behavior in amphetamine-treated rats
Authors:	Hsieh, Yih-Shou Chen, Pei-Ni Yu, Ching-Han Liao, Jiuan-Miaw Kuo, Dong-Yih
Contributors:	中山醫學大學
Keywords:	NPY-Y1 receptor;c-Fos;c-Jun;AP-1;Appetite;Hypothalamus
Date:	2013
Issue Date:	2015-07-21T04:40:53Z (UTC)
Abstract:	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.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11433
Appears in Collections:	[The Institute of Biochemistry, Microbiology and Immunology ] Journal Paper

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