Increased feeding after treatment with fructose, but not glucose, antimetabolites in rats with dopamine-depleting brain lesions.
Rats were given dopamine-depleting lesions either as adults or as neonates. Compared with intact controls, lesioned rats failed to increase their food intake after acute administration of the glucoprivic agent, 2-deoxy-D-glucose. In contrast, both lesioned and control rats increased food intake after acute treatment with a peripherally-acting fructose antimetabolite, 2,5-anhydro-D-mannitol. These data suggest that the failure of lesioned rats to respond behaviorally to glucoprivation is related to inhibition of glycolysis in the brain, rather than the acute nature of the metabolic challenge.
Department of Psychology, University of Florida, Gainesville 32611-2065.
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Rowland
D000818:Animals; D000963:Antimetabolites / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects / Q000502:physiology*; D003847:Deoxyglucose / Q000494:pharmacology*; D004298:Dopamine / Q000502:physiology*; D005247:Feeding Behavior / Q000187:drug effects*; D005260:Female; D007276:Injections, Intraventricular; D008297:Male; D008353:Mannitol / Q000031:analogs & derivatives* / Q000494:pharmacology; D016627:Oxidopamine; D051381:Rats; D017207:Rats, Sprague-Dawley
D000963:Antimetabolites; D008353:Mannitol; C031765:2,5-anhydromannitol; D016627:Oxidopamine; D003847:Deoxyglucose; D004298:Dopamine