title: Enhanced feeding response to neuropeptide Y in hypothalamic neuropeptide Y-depleted rats.
abstract: Monosodium glutamate is neurotoxic for the arcuate nucleus and more generally for all circumventricular organs when injected in newborn rats. Neuropeptide Y, a potent stimulator of food intake, is mainly synthesized in the arcuate nucleus. In the present experiment, we determined the hypothalamic status and the feeding response to intracerebroventricular neuropeptide Y in adult rats neonatally treated with monosodium glutamate. Marked neuropeptide Y decreases were measured in the arcuate nucleus and in the paraventricular nuclei in monosodium glutamate-treated rats (-40%; P < 0.01). Adult rats neonatally treated with monosodium glutamate weighed significantly less (-8%; P < 0.01) and ate less (-10%; P < 0.01) than the control rats. Neuropeptide Y injections in a lateral brain ventricle stimulated food intake in control and monosodium glutamate-treated rats in a dose-dependent manner (P < 0.001). Whatever the time after drug injection (2, 4, 6 and 8 h) and the injected dose (0.5, 1 and 5 micrograms), feeding responses were always greater in monosodium glutamate-treated rats (about 2 times greater starting with the lowest dose (0.5 microgram): 9.3 +/- 1.0 (monosodium glutamate) vs. 5.3 +/- 0.7 (control) g/2 h, P < 0.01). Calculated minimal effective doses were also always smaller in monosodium glutamate-treated rats than in control animals (P < 0.01). Neuropeptide Y increased meal duration, meal size and decreased latency to initiate feeding in monosodium glutamate-treated rats (P < 0.01) and control rats (P < 0.01). For each dose of neuropeptide Y, effects were more pronounced on meal size (+70%) and meal duration (+25%) in monosodium glutamate-treated rats than in control rats. Therefore, monosodium glutamate-treated rats were more sensitive to exogenous neuropeptide Y. Decreased food intake in the monosodium glutamate-treated rats was associated with a decrease in neuropeptide Y concentrations in the arcuate-paraventricular axis. This confirms the functional role of this peptidergic pathway in eating behavior.
authors.affiliation: INSERM U-308, MRCA, Equipe de Neurobiologie et Physiologie Expérimentales, Nancy, France.
authors.forename: A
authors.initials: A
authors.lastname: Stricker-Krongrad
authors.forename: B
authors.initials: B
authors.lastname: Beck
authors.forename: C
authors.initials: C
authors.lastname: Burlet
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D004305:Dose-Response Relationship, Drug; D004435:Eating / Q000187:drug effects*; D007031:Hypothalamus / Q000187:drug effects*; D009478:Neuropeptide Y / Q000494:pharmacology*; D051381:Rats; D012970:Sodium Glutamate / Q000494:pharmacology; D014018:Tissue Distribution
chemical_list: D009478:Neuropeptide Y; D012970:Sodium Glutamate