The forebrain is not essential for sympathoadrenal hyperglycemic response to glucoprivation.
The reduction of glycolysis by hypoglycemia or the glucose analog 2-deoxy-D-glucose (2DG) stimulates compensatory sympathetic alterations of metabolism. Considerable attention has been focused on the hypothalamus as the probable locus of requisite metabolic signal detection. We report, however, that unanesthetized chronically decerebrate rats are capable of exhibiting sympathoadrenal hyperglycemia in response to the metabolic challenge presented by 2DG. This findings demonstrates that the forebrain is not necessary for glucoprivic stimulation of this reflex. Since cervical cord transection has been shown to eliminate hyperglycemia induced by 2DG, we conclude that the caudal brainstem contains an essential part of the neural mechanism which both detects metabolic need and ameliorates that need through the release of stored fuels.
D000311:Adrenal Glands / Q000502:physiology; D000344:Afferent Pathways; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001933:Brain Stem / Q000502:physiology*; D003655:Decerebrate State; D003837:Deoxy Sugars / Q000494:pharmacology*; D003847:Deoxyglucose / Q000494:pharmacology*; D004734:Energy Metabolism; D007031:Hypothalamus / Q000502:physiology*; D051381:Rats; D012018:Reflex / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology
D001786:Blood Glucose; D003837:Deoxy Sugars; D003847:Deoxyglucose