Abstract
Fever is a result of the action of prostaglandin E2 (PGE2) on the brain and appears to require EP3 prostaglandin receptors (EP3Rs), but the specific neurons on which PGE2 acts to produce fever have not been definitively established. Here we report that selective genetic deletion of the EP3Rs in the median preoptic nucleus of mice resulted in abrogation of the fever response. These observations demonstrate that the EP3R-bearing neurons in the median preoptic nucleus are required for fever responses.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Body Temperature / drug effects
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Body Temperature / genetics
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Body Temperature / physiology
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Dinoprostone / pharmacology
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Fever* / chemically induced
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Fever* / genetics
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Gene Expression Regulation / drug effects
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Gene Expression Regulation / genetics
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Green Fluorescent Proteins / metabolism
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In Situ Hybridization / methods
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Mice
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Mice, Knockout
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Neurons / drug effects
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Neurons / physiology*
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Preoptic Area / cytology
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Preoptic Area / physiology*
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Receptors, Prostaglandin E / deficiency
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Receptors, Prostaglandin E / metabolism*
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Receptors, Prostaglandin E, EP3 Subtype
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Time Factors
Substances
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Ptger3 protein, mouse
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Receptors, Prostaglandin E
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Receptors, Prostaglandin E, EP3 Subtype
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Green Fluorescent Proteins
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Dinoprostone