Source:http://linkedlifedata.com/resource/pubmed/id/15718385
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2005-5-11
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pubmed:abstractText |
Evidence in rats suggests that central oxytocin (OT) signaling pathways contribute to suppression of food intake during dehydration (i.e., dehydration anorexia). The present study examined water deprivation-induced dehydration anorexia in wild-type and OT -/- mice. Mice were deprived of food alone (fasted, euhydrated) or were deprived of both food and water (fasted, dehydrated) for 18 h overnight. Fasted wild-type mice consumed significantly less chow during a 60-min refeeding period when dehydrated compared with their intake when euhydrated. Conversely, fasting-induced food intake was slightly but not significantly suppressed by dehydration in OT -/- mice, evidence for attenuated dehydration anorexia. In a separate experiment, mice were deprived of water (but not food) overnight for 18 h; then they were anesthetized and perfused with fixative for immunocytochemical analysis of central Fos expression. Fos was elevated similarly in osmo- and volume-sensitive regions of the basal forebrain and hypothalamus in wild-type and OT -/- mice after water deprivation. OT-positive neurons expressed Fos in dehydrated wild-type mice, and vasopressin-positive neurons were activated to a similar extent in wild-type and OT -/- mice. Conversely, significantly fewer neurons within the hindbrain dorsal vagal complex were activated in OT -/- mice after water deprivation compared with activation in wild-type mice. These findings support the view that OT-containing projections from the hypothalamus to the hindbrain are necessary for the full expression of compensatory behavioral and physiological responses to dehydration.
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pubmed:grant | |
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 |
Jun
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pubmed:issn |
0363-6119
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
288
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
R1791-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:15718385-Animals,
pubmed-meshheading:15718385-Anorexia,
pubmed-meshheading:15718385-Blood Volume,
pubmed-meshheading:15718385-DNA,
pubmed-meshheading:15718385-Dehydration,
pubmed-meshheading:15718385-Eating,
pubmed-meshheading:15718385-Food Deprivation,
pubmed-meshheading:15718385-Genotype,
pubmed-meshheading:15718385-Hindlimb,
pubmed-meshheading:15718385-Immunohistochemistry,
pubmed-meshheading:15718385-Male,
pubmed-meshheading:15718385-Mice,
pubmed-meshheading:15718385-Mice, Inbred C57BL,
pubmed-meshheading:15718385-Mice, Knockout,
pubmed-meshheading:15718385-Oxytocin,
pubmed-meshheading:15718385-Proto-Oncogene Proteins c-fos,
pubmed-meshheading:15718385-Rhombencephalon,
pubmed-meshheading:15718385-Vasopressins
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pubmed:year |
2005
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pubmed:articleTitle |
Dehydration anorexia is attenuated in oxytocin-deficient mice.
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pubmed:affiliation |
University of Pittsburgh, Department of Neuroscience, 446 Crawford Hall, Pittsburgh, PA 15260, USA. Rinaman@pitt.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, N.I.H., Extramural
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