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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1996-10-29
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pubmed:abstractText |
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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0014-2999
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
4
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pubmed:volume |
295
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
27-34
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8925871-Animals,
pubmed-meshheading:8925871-Animals, Newborn,
pubmed-meshheading:8925871-Dose-Response Relationship, Drug,
pubmed-meshheading:8925871-Eating,
pubmed-meshheading:8925871-Hypothalamus,
pubmed-meshheading:8925871-Neuropeptide Y,
pubmed-meshheading:8925871-Rats,
pubmed-meshheading:8925871-Sodium Glutamate,
pubmed-meshheading:8925871-Tissue Distribution
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pubmed:year |
1996
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pubmed:articleTitle |
Enhanced feeding response to neuropeptide Y in hypothalamic neuropeptide Y-depleted rats.
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pubmed:affiliation |
INSERM U-308, MRCA, Equipe de Neurobiologie et Physiologie Expérimentales, Nancy, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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