Abstract
Previous studies showed that lesions of the lateral or ventromedial hypothalamus impair sodium appetite but that lesions of the anterior or posterior medial forebrain bundle or periventricular system which carry hypothalamofugal fibers have no observable effect. In the present study other known or potential hypothalamofugal pathways were disjoined with no observable effect upon sodium appetite. Lateral hypothalamic lesions completely abolished sodium appetite under the same experimental conditions. It was concluded that no single neural pathway is necessary for transmission of hypothalamic natrorectic functions. In addition to data on sodium appetite, observations on disturbances of feeding behavior following certain subthalamic lesions are described, and motor and motivational functions of the subthalamus and hypothalamus are discussed.
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