Acute homeostatic imbalances reinstate sensorimotor dysfunctions in rats with lateral hypothalamic lesions.

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Abstract
It was previously demonstrated that rats recovered from aphagia and adipsia after large bilateral electrolytic lesions of the lateral hypothalamic area did not show the normal feeding response to 2-deoxyglucose or drinking response to polyethylene glycol. Such homeostatic imbalances reinstate the profound sensorimotor impairments that are seen in the immediate postoperative period but abate in parallel with the gradual recovery of ingestive behaviors. Administration of .alpha.-methyltyrosine or spiroperidol produced senosry and motor dysfunctions in rats with lateral hypothalamic lesions that were similar to those observed after 2-deoxyglucose. The residual feeding and drinking deficits of rats with lateral hypothalamic lesions after apparent recovery of function do not reflect specific loss of putative gluco- and volume-regulatory contributions to ingestive behavior. They may indicate continued impairments in nonspecific activational components of motivation that normally are mediated, in part, by central dopaminergic neurons.

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