ArticleMolecular brain2013
The neuropeptide Y Y1 receptor knockdown modulates activator protein 1-involved feeding behavior in amphetamine-treated rats.
Article in Molecular brain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Therapeutic potential of modulating endogenous PYY expression for controlling overweight and obesity: a narrative review.Frontiers in nutrition · 2026Review
- Phylogenetic conservation of the interdependent homeostatic relationship of sleep regulation and redox metabolism.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2024Review
- Prognostic and Functional Analysis ofDisease markers · 2022Article
- Y1 receptors modulate taste-related behavioral responsiveness in male mice to prototypical gustatory stimuli.Hormones and behavior · 2021Article
- Lack of Spinal Neuropeptide Y Is Involved in Mechanical Itch in Aged Mice.Frontiers in aging neuroscience · 2021Article
- Neuropeptides Exert Neuroprotective Effects in Alzheimer's Disease.Frontiers in molecular neuroscience · 2018Review
- Characterization and expression analysis of two distinct neuropeptide Ya paralogues in Jian carp (Cyprinus carpio var. Jian).Fish physiology and biochemistry · 2014Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypothalamic 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.
methodsRats 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.
resultsDecreased 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.
conclusionsThese 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.
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