The effect of estrogen replacement on several parameters of energy balance was investigated in ovariectomized rats tested during the dark phase of their diurnal cycle. Estrogen replacement, either as 17 beta-estradiol or beta-estradiol-3-benzoate via subcutaneous Silastic capsules, was associated with elevated rates of heat production and dry heat loss relative to untreated ovariectomized controls. Estrogen treatment reduced body mass and retarded fur growth. The effects of estrogen replacement on heat production and dry heat loss could not be attributed to these differences in body mass and fur growth or locomotor activity. Estrogen replacement had no effect on rate of evaporative heat loss. If estrogen replacement was delayed 75 days following ovariectomy, the increase in heat production and dry heat loss was not observed. There was no effect of the hormone treatment on rectal temperature. It was concluded that either heat production was elevated, with dry heat loss increased to compensate for the additional thermal load, or dry heat loss was accelerated with heat production elevated in compensation.

Hyperphagic, aphagio, and aphagie-hyperphagic rats showed evidence of caloric tracking when presented with diets varying independently in caloric density and palatability, even though the accuracy of caloric regulation was severely impaired by the hypothalamic lesions and consequent change in diet preference. Although palatability was a potent determinant of food intake in operated animals, caloric tracking could not be accounted for on the basis of palatability preferences. Greasy diets were preferred to pellets regardless of the caloric density of the diet, but the calorically denser diet was preferred if the greasy texture was held constant. Normal rats maintained a relatively constant caloric intake when the diet was varied over a wide caloric and textural range.

Amphetamine sulphate produced significantly greater depression of food intake in normal rats than in rats with lateral hypothalamic lesions, suggesting that amphetamine reduces food intake by inhibiting the lateral hypothalamus. The 2 groups did not differ significantly with respect to the action of amphetamine on water intake (suggesting different central sites of action of this drug for food and water intake) or with respect to water intake following injections of chlorpromazine HC1 or neostigmine methylsulfate.

The ability of rats to regulate body temperature in a cold environment by behavioral means following hypothalamic lesions was studied using a heat-reinforced operant procedure. The most consistent consequence of preoptic and anterior lesions was an increased rate of response for radiant heat reinforcement; in spite of this, posttest rectal temperature was often low. Transient or minor changes were noted in some Ss with preoptic or anterior lesions, and in those with posterior and septal lesions. These data indicate that (a) deficits in physiological regulation in the cold can be obtained following rostral hypothalamic damage, (6) the effective lesion site is primarily but not exclusively the medial preoptic region, and (c) behavioral compensation for an impaired regulatory ability occurs.

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