Experimental hyperphagia in cats following destructive mid‐brain lesions

Abstract

Cats were given an "ad-lib" diet before and after attempted electrolytic destruction of the periaqueductal gray matter beneath the superior colliculus. Daily records were kept of their caloric intake and weight. Seven animals became hyperphagic. Six remained so until the end of the experimental period and 1 did not. Five animals, including the one that did not remain hyperphagic, had destructive lesions which involved the dorsal periaqueductal gray matter and adjacent tectum and tegmentum. The other 2 had smaller ventral lesions which involved the ventrolateral edge of the periaqueductal gray matter and the adjacent tegmentum. One cat with less extensive destruction of the periaqueductal gray matter and one with more extensive ventral destructive lesions did not become hyperphagic. Among the cats which became hyperphagic, 2 different patterns of relationship between weight gain and caloric intake were demonstrated; however, these did not correlate directly with the 2 different types of lesions. Destructive lesions of a sufficient quantity of the dorsal periaqueductal gray matter and adjacent tissue are followed by hyperphagia in adult cats; also, minimal destructive lesions of the more ventral periaqueductal gray matter and adjacent tissue are followed by hyperphagia. In view of the disparate sites of bilateral mesencephalic lesions attended by hyperphagia (namely, dorsal and ventral periaqueductal gray matter, lateral mesencephalic tegmentum, and rostral-ventral mescencephalic tegmentum) we infer that no 1:1 correspondence prevails between an "anatomic center " in the midbrain and euphagia. In view of the results of our investigations and the material cited from the literature, we conclude that there are anumber of destructive lesions of the central nervous system which bring about a disturbance of relationship among (unknown) structural-functional components which usually, but not always, result in hyperphagia.