| pubmed-article:8779877 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8779877 | lifeskim:mentions | umls-concept:C0920298 | lld:lifeskim |
| pubmed-article:8779877 | lifeskim:mentions | umls-concept:C0020663 | lld:lifeskim |
| pubmed-article:8779877 | lifeskim:mentions | umls-concept:C0205093 | lld:lifeskim |
| pubmed-article:8779877 | lifeskim:mentions | umls-concept:C0080093 | lld:lifeskim |
| pubmed-article:8779877 | lifeskim:mentions | umls-concept:C0013470 | lld:lifeskim |
| pubmed-article:8779877 | lifeskim:mentions | umls-concept:C0220839 | lld:lifeskim |
| pubmed-article:8779877 | lifeskim:mentions | umls-concept:C0205463 | lld:lifeskim |
| pubmed-article:8779877 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:8779877 | lifeskim:mentions | umls-concept:C1363844 | lld:lifeskim |
| pubmed-article:8779877 | pubmed:issue | 2 Pt 2 | lld:pubmed |
| pubmed-article:8779877 | pubmed:dateCreated | 1996-12-20 | lld:pubmed |
| pubmed-article:8779877 | pubmed:abstractText | To determine whether endogenous lateral hypothalamic (LH) glutamate and its N-methyl-D-aspartate (NMDA) receptors might participate in the stimulation of natural eating, LH injection of the NMDA antagonist D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5) was tested in adult male rats for suppressive actions on feeding elicited by 1) NMDA, kainic acid or D, L-alpha-amino-3-hydroxy-5-methylisoxazole (AMPA) injected into the LH; 2) food deprivation; and 3) the onset of the nocturnal period. D-AP5 (10-100 nmol) reduced by 72-90% the approximately 10-g eating response elicited by NMDA (10 nmol) without affecting the quantitatively similar eating responses elicited by kainic acid (1.0 nmol) or AMPA (1.0 nmol). This treatment also suppressed deprivation-induced eating by as much as 61% and nocturnal eating by as much as 40%. To determine its long-term effects, D-AP5 (50 nmol) was injected bilaterally into the LH twice a day for 8 consecutive days. This treatment caused up to 65% reductions in daily food intake and body weight loss of up to 13 g/day. These findings, showing behaviorally selective suppressions of eating and body weight by D-AP5, argue that endogenous LH glutamate acts to regulate natural eating and body weight and that NMDA receptors participate in these functions. | lld:pubmed |
| pubmed-article:8779877 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8779877 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8779877 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8779877 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8779877 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8779877 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8779877 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8779877 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8779877 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:8779877 | pubmed:author | pubmed-author:StanleyB GBG | lld:pubmed |
| pubmed-article:8779877 | pubmed:author | pubmed-author:WillettV... | lld:pubmed |
| pubmed-article:8779877 | pubmed:author | pubmed-author:DoniasH WHW | lld:pubmed |
| pubmed-article:8779877 | pubmed:author | pubmed-author:DeeM GMG2nd | lld:pubmed |
| pubmed-article:8779877 | pubmed:author | pubmed-author:DuvaM AMA | lld:pubmed |
| pubmed-article:8779877 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8779877 | pubmed:volume | 270 | lld:pubmed |
| pubmed-article:8779877 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8779877 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8779877 | pubmed:pagination | R443-9 | lld:pubmed |
| pubmed-article:8779877 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:8779877 | pubmed:meshHeading | pubmed-meshheading:8779877-... | lld:pubmed |
| pubmed-article:8779877 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8779877 | pubmed:articleTitle | Lateral hypothalamic NMDA receptors and glutamate as physiological mediators of eating and weight control. | lld:pubmed |
| pubmed-article:8779877 | pubmed:affiliation | Department of Neuroscience, University of California, Riverside 92521, USA. | lld:pubmed |
| pubmed-article:8779877 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8779877 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8779877 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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