Abstract

Neurologically intact rats were presented with a 0.2% (w/v) quinine adulterated water supply, and they failed to meter fluid consumption homeostatically in accordance with the elevated food intake that followed glucoprivation induced by 250, 500, and 750 mg/kg injections of 2-deoxy-D-glucose (2DG). These animals, nevertheless, were statistically indistinguishable from controls in the amount of food eaten following the 2DG treatments. These data suggest that the hypodipsia produced by some brain lesions is not a sufficient stimulus to produce the deficient glucoprivic feeding that accompanies such lesions; therefore, future lesion investigations that simultaneously yield hypodipsia and reduced eating in response to 2DG need not employ hypodipsic neurologically intact controls.

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