Abstract
Electrolytic lesions of the posteromedial portion of the ventrobasal thalamic complex of rats impaired the feeding response to glucoprivation produced by systemic injection of 2-deoxy-D-glucose and the sodium appetite induced by injections of desoxycorticosterone, and produced abnormally low water intake in the absence of food. Drinking elicited by intracellular dehydration was not consistently affected. Lesions of the ventral anterior nucleus of the thalamus only impaired the feeding response to glucoprivation. The behavioral changes observed after posterior ventrobasal thalamic damage may be related to a disruption of gustatory, visceral, and somatosensory thalamic connections with the corpus striatum and neocortex.
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