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May 1966

Changes in Caloric Intake Following Brain Stem Lesions in Cats: II. Effects of Lesions in Medial Hypothalamic Region*

Author Affiliations

From the Division of Neurosurgery, University of Iowa College of Medicine, Iowa City.

Arch Neurol. 1966;14(5):541-552. doi:10.1001/archneur.1966.00470110085011

THE DEVELOPMENT of obesity or hyperphagia or both following lesions in the region of the hypothalamus has been reported in rats,1-5 mice,6,7 dogs,8-10 cast,1,11-13 and monkeys.11,14-17 Most lesions were produced by electrolysis in the general region of the hypothalamic ventromedial nuclei bilaterally. However, Bailey and Bremer8 reported that their lesions were in the posterior hypothalamus in dogs; and Heinbecker et al9 reported that their lesions, also in dogs, were in the paraventricular nuclei. Mayer6 produced hyperphagia and obesity in mice by feeding aurothioglucose.

The assumption that bilateral destruction of the ventromedial hypothalamic nuclei constitute the essential lesion is not unequivocally established in the literature. Brobeck et al2 reported hyperphagia and obesity in albino rats after lesions in the ventromedial region of the hypothalamus in which the ventromedial nuclei were not destroyed bilaterally. Kennedy5 produced hyperphagic rats with hypothalamic lesions

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