THE BRAIN LESION OF GOLDTHIOGLUCOSE OBESITY

Author:

Brecher G.1,Laqueur G. L.1,Cronkite E. P.1,Edelman P. M.1,Schwartz I. L.1

Affiliation:

1. From the National Institute of Arthritis and Metabolic Disease, National Institutes of Health, Bethesda, the Medical Research Center, Brookhaven National Laboratory, Upton, New York, and the Department of Physiology, University of Cincinnati College of Medicine, Cincinnati

Abstract

The development of hypothalamic lesions due to goldthioglucose are described. The initial extensive necrotic lesion occurs in close to 100 per cent of animals injected with LD50. Within 2 weeks the necrotic material has been removed and a narrow scar results. After a lapse of several months, the scar is often difficult to visualize, especially in animals that have not developed obesity. The ventromedial nucleus is not the center of the lesion. The nucleus is preserved in some instances, and partially or completely destroyed in others, depending on the extent of the lesion. The more prominent scar in the obese animals correlates with the larger initial lesion necessary for the complete bilateral destruction of the ventromedial nucleus which is known to be a prerequisite for the development of hypothalamic obesity. Thus, contrary to earlier suggestions, goldthioglucose does not localize specifically in the cells of the ventromedial nucleus.

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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