Facilitation of Recovery after Lateral Hypothalamic Damage by Prior Ablation of Frontal Cortex

Abstract

BILATERAL lesions of the lateral hypothalmus in the rat produce aphagia and adipsia¹, but if the animals are kept alive by intragastric feeding they may begin to eat and drink spontaneously again after a few days^1–4. It has been suggested⁵ that recovery of feeding depends on the recovery of an adrenergic reward system, partial denervation of which may account for less severe deficits in feeding behaviour after other lesions of the central nervous system. For example, ablation of frontal cortex in the rat results in progressive loss of weight for 3–4 days, followed by recovery⁶, and also in changed sensitivities to drugs affecting noradrenergic synapses^7,8. It seems possible that denervation supersensitivity may be the explanation of the recovery of function^8,9. We suggest that lateral hypothalamic lesions may partially denervate hypothalamic neurones as a result of the destruction of intrahypothalamic connexions. Thus if lateral hypothalamic neurones were partially denervated by ablation of frontal cortex at some time before damage to the lateral hypothalamus itself, delayed supersensitivity from the cortical lesion should result in facilitated recovery. We now present data to support this hypothesis.