Involvement of neuropeptide Y Y1 receptor in the regulation of amphetamine-mediated appetite suppression

Dong-Yih Kuo; Pei-Ni Chen; Ching-Han Yu; Meng-Hsien Kuo; Yih-Shou Hsieh; Shu-Chen Chu

doi:10.1016/j.neuropharm.2012.06.018

Involvement of neuropeptide Y Y1 receptor in the regulation of amphetamine-mediated appetite suppression

Neuropharmacology. 2012 Oct;63(5):842-50. doi: 10.1016/j.neuropharm.2012.06.018. Epub 2012 Jun 22.

Authors

Dong-Yih Kuo¹, Pei-Ni Chen, Ching-Han Yu, Meng-Hsien Kuo, Yih-Shou Hsieh, Shu-Chen Chu

Affiliation

¹ Department of Physiology, Chung Shan Medical University and Chung Shan Medical University Hospital, Taichung City 40201, Taiwan, ROC. dykuo@csmu.edu.tw

PMID: 22732442
DOI: 10.1016/j.neuropharm.2012.06.018

Abstract

Recently, we reported that an initial decrease followed by recovery of food intake was observed during four days of amphetamine (AMPH) treatment and suggested that these changes in response were mediated by changes in neuropeptide Y (NPY) and proopiomelanocortin (POMC). Here we investigated if Y1 receptor (Y1R) and/or Y5 receptor (Y5R) might be involved in this regulation. Rats were treated daily with AMPH for four days. Changes in the expression levels of Y1R, Y5R, melanocortin receptor 3 (MC3R), and NPY were assessed and compared. Results showed that Y1R and MC3R increased, with a maximal increase of about 210% on Day 2 but with a restoration to the normal level on Day 4. In contrast, NPY decreased with a biggest reduction of about 45% on Day 2 and the pattern of expression during AMPH treatment was opposite to those of Y1R and MC3R, while the expression of Y5R was not changed. Central inhibitions of NPY formation or Y1R activity modulated the anorectic response of AMPH and the reciprocal regulation of NPY and MC3R, revealing a crucial role of Y1R in this action. It is suggested that Y1R participates in the reciprocal regulation of NPY- and MC3R-containing neurons in the hypothalamus during the anorectic effect of AMPH. These results may further the understanding of Y1R in the control of eating.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Amphetamine / administration & dosage
Amphetamine / antagonists & inhibitors
Amphetamine / pharmacology*
Animals
Appetite Depressants / administration & dosage
Appetite Depressants / chemistry
Appetite Depressants / pharmacology*
Appetite Regulation / drug effects*
Behavior, Animal / drug effects
Dopamine Antagonists / pharmacology
Dose-Response Relationship, Drug
Drug Tolerance*
Eating / drug effects
Gene Expression Regulation / drug effects
Haloperidol / pharmacology
Hypothalamus / drug effects*
Hypothalamus / metabolism
Male
Nerve Tissue Proteins / antagonists & inhibitors
Nerve Tissue Proteins / genetics
Nerve Tissue Proteins / metabolism
Neurons / drug effects*
Neurons / metabolism
Neuropeptide Y / antagonists & inhibitors
Neuropeptide Y / genetics
Neuropeptide Y / metabolism
Oligonucleotides, Antisense
Rats
Rats, Wistar
Receptor, Melanocortin, Type 3
Receptors, Melanocortin / metabolism
Receptors, Neuropeptide Y / antagonists & inhibitors
Receptors, Neuropeptide Y / metabolism*

Substances

Appetite Depressants
Dopamine Antagonists
Nerve Tissue Proteins
Neuropeptide Y
Oligonucleotides, Antisense
Receptor, Melanocortin, Type 3
Receptors, Melanocortin
Receptors, Neuropeptide Y
melanocortin 3 receptor, rat
neuropeptide Y-Y1 receptor
neuropeptide Y5 receptor
Amphetamine
Haloperidol