The interaction of clonidine and nitric oxide on feeding behavior in the chicken

Yang Ho Choi, Mitsuhiro Furuse, Jun ichi Okumura, D. Michael Denbow

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Central administration ofα2-receptor agonists stimulate food intake in mammalian and avian species. Recently we reported that inhibition of nitric oxide (NO) synthase (NOS) decreased food intake in chickens. In the present study, we investigated whether the increased eating induced by clonidine (Clon), andα2-receptor agonist, is attenuated by NOS inhibition. In the first experiment, four levels (0, 9.4, 18.8 or 37.5 nmol/10 μl) of Clon were administered into the right lateral ventricle of chickens, and food intake was monitored. Clon increased 30 min-food intake in a dose-dependent manner. In a co-administration study ofl-NG-nitro-arginine methyl ester HCl (LNNA), a NOS inhibitor, and Clon, LNNA (0, 1.5, 3.0 or 5.9 μmol) attenuated food intake induced by Clon (37.5 nmol) in a dose-dependent manner. Our results suggest the possibility that NO interacts with adrenergic neurons in the central nervous system to modulate feeding behavior in the chicken.

Original languageEnglish
Pages (from-to)161-164
Number of pages4
JournalBrain Research
Volume699
Issue number1
DOIs
Publication statusPublished - Nov 13 1995
Externally publishedYes

Fingerprint

Clonidine
Feeding Behavior
Chickens
Nitric Oxide
Eating
Nitric Oxide Synthase
Adrenergic Neurons
Lateral Ventricles
Heart Ventricles
Central Nervous System

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Developmental Biology
  • Clinical Neurology

Cite this

The interaction of clonidine and nitric oxide on feeding behavior in the chicken. / Choi, Yang Ho; Furuse, Mitsuhiro; Okumura, Jun ichi; Michael Denbow, D.

In: Brain Research, Vol. 699, No. 1, 13.11.1995, p. 161-164.

Research output: Contribution to journalArticle

Choi, Yang Ho ; Furuse, Mitsuhiro ; Okumura, Jun ichi ; Michael Denbow, D. / The interaction of clonidine and nitric oxide on feeding behavior in the chicken. In: Brain Research. 1995 ; Vol. 699, No. 1. pp. 161-164.
@article{15de8dc930424d8aba6baa525e84f134,
title = "The interaction of clonidine and nitric oxide on feeding behavior in the chicken",
abstract = "Central administration ofα2-receptor agonists stimulate food intake in mammalian and avian species. Recently we reported that inhibition of nitric oxide (NO) synthase (NOS) decreased food intake in chickens. In the present study, we investigated whether the increased eating induced by clonidine (Clon), andα2-receptor agonist, is attenuated by NOS inhibition. In the first experiment, four levels (0, 9.4, 18.8 or 37.5 nmol/10 μl) of Clon were administered into the right lateral ventricle of chickens, and food intake was monitored. Clon increased 30 min-food intake in a dose-dependent manner. In a co-administration study ofl-NG-nitro-arginine methyl ester HCl (LNNA), a NOS inhibitor, and Clon, LNNA (0, 1.5, 3.0 or 5.9 μmol) attenuated food intake induced by Clon (37.5 nmol) in a dose-dependent manner. Our results suggest the possibility that NO interacts with adrenergic neurons in the central nervous system to modulate feeding behavior in the chicken.",
author = "Choi, {Yang Ho} and Mitsuhiro Furuse and Okumura, {Jun ichi} and {Michael Denbow}, D.",
year = "1995",
month = "11",
day = "13",
doi = "10.1016/0006-8993(95)01057-3",
language = "English",
volume = "699",
pages = "161--164",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - The interaction of clonidine and nitric oxide on feeding behavior in the chicken

AU - Choi, Yang Ho

AU - Furuse, Mitsuhiro

AU - Okumura, Jun ichi

AU - Michael Denbow, D.

PY - 1995/11/13

Y1 - 1995/11/13

N2 - Central administration ofα2-receptor agonists stimulate food intake in mammalian and avian species. Recently we reported that inhibition of nitric oxide (NO) synthase (NOS) decreased food intake in chickens. In the present study, we investigated whether the increased eating induced by clonidine (Clon), andα2-receptor agonist, is attenuated by NOS inhibition. In the first experiment, four levels (0, 9.4, 18.8 or 37.5 nmol/10 μl) of Clon were administered into the right lateral ventricle of chickens, and food intake was monitored. Clon increased 30 min-food intake in a dose-dependent manner. In a co-administration study ofl-NG-nitro-arginine methyl ester HCl (LNNA), a NOS inhibitor, and Clon, LNNA (0, 1.5, 3.0 or 5.9 μmol) attenuated food intake induced by Clon (37.5 nmol) in a dose-dependent manner. Our results suggest the possibility that NO interacts with adrenergic neurons in the central nervous system to modulate feeding behavior in the chicken.

AB - Central administration ofα2-receptor agonists stimulate food intake in mammalian and avian species. Recently we reported that inhibition of nitric oxide (NO) synthase (NOS) decreased food intake in chickens. In the present study, we investigated whether the increased eating induced by clonidine (Clon), andα2-receptor agonist, is attenuated by NOS inhibition. In the first experiment, four levels (0, 9.4, 18.8 or 37.5 nmol/10 μl) of Clon were administered into the right lateral ventricle of chickens, and food intake was monitored. Clon increased 30 min-food intake in a dose-dependent manner. In a co-administration study ofl-NG-nitro-arginine methyl ester HCl (LNNA), a NOS inhibitor, and Clon, LNNA (0, 1.5, 3.0 or 5.9 μmol) attenuated food intake induced by Clon (37.5 nmol) in a dose-dependent manner. Our results suggest the possibility that NO interacts with adrenergic neurons in the central nervous system to modulate feeding behavior in the chicken.

UR - http://www.scopus.com/inward/record.url?scp=0028822850&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028822850&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(95)01057-3

DO - 10.1016/0006-8993(95)01057-3

M3 - Article

C2 - 8616609

AN - SCOPUS:0028822850

VL - 699

SP - 161

EP - 164

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -