title: Glutamatergic control of food intake in pigeons: effects of central injections of glutamate, NMDA, and AMPA receptor agonists and antagonists.
abstract: The possible involvement of glutamatergic mechanisms in the control of food intake was studied in free-feeding and in 24-h food-deprived (FD24) pigeons for 1 h after intracerebroventricular (i.c.v.) treatment with glutamate (Glu, 0, 50, 150, 300, and 600 nmol). Glu injections dose dependently induced decreases (30-65%) in food intake (FI) and feeding duration (FD), and increases in latency to start feeding (LSF) in FD24 animals, but not in free-feeding ones. None of these treatments affected noningestive behaviors (locomotion, sleep, and preening). In FD24 pigeons, i.c.v. treatments with N-methyl-D-aspartic acid (NMDA, 0.1, 1, 4, 8, or 16 nmol) or D,L-alpha-amino-3-hydroxy-isoxazole proprionic acid (AMPA, 0.1, 1, 4, or 8 nmol) decreased FI and FD, but left LSF unchanged compared to vehicle-treated FD24 controls. Kainic acid (0.1, 0.5, and 1 nmol), or [trans-(1S,3R)-ACPD-(5NH4OH)] (ACPD, 0.1, 1, 4, 8, and 16 nmol) left unchanged the ingestive profile of FD24 pigeons. Pretreatment with the NMDA receptor antagonist MK-801 (15 nmol) and the AMPA-kainate receptor antagonist CNQX (390 nmol), 20 min before an i.c.v. injection of Glu (300 nmol) induced a partial blockade of the Glu-induced decreases in FI and FD and completely inhibited the Glu-induced increase in LSF in FD24 pigeons. I.c.v. injections of MK-801 (30 nmol) and of CNQX (780 nmol) increased FI and FD and reduced LSF in free-feeding pigeons. A lower dose of MK-801 (15 nmol) increased FI and FD, but not LSF. Conversely, a lower dose of CNQX (390 nmol) reduced LSF without changing FI or FD. These findings indicate the involvement of Glu as a chemical mediator in the regulation of food intake in the pigeon, possibly acting on multiple central mechanisms in this species through NMDA- and AMPA-sensitive Glu receptors.
authors.affiliation: Department of Physiological Sciences, Center of Biological Sciences, Federal University of Santa Catarina, Florianopolis, Brazil.
authors.forename: L A
authors.initials: LA
authors.lastname: Zeni
authors.forename: H B
authors.initials: HB
authors.lastname: Seidler
authors.forename: N A
authors.initials: NA
authors.lastname: De Carvalho
authors.forename: C G
authors.initials: CG
authors.lastname: Freitas
authors.forename: J
authors.initials: J
authors.lastname: Marino-Neto
authors.forename: M A
authors.initials: MA
authors.lastname: Paschoalini
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000187:drug effects*; D010856:Columbidae; D004305:Dose-Response Relationship, Drug; D004435:Eating / Q000187:drug effects*; D018698:Glutamic Acid / Q000494:pharmacology*; D007276:Injections, Intraventricular; D008297:Male; D018091:Receptors, AMPA / Q000502:physiology*; D017470:Receptors, Glutamate / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*
chemical_list: D018091:Receptors, AMPA; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione