The immediate development of behavioral and biochemical changes following ventromedial hypothalamic lesions in rats

Development of acute feeding disorders, hyperactivity, and stomach pathology after medial and lateral hypothalamic lesions in rats

“…The long-term hyperphagia and weight gain which are characteristic of the classic VMH syndrome have also been observed in this laboratory with the lesion procedure used in the present acute experiments. However, insofar as acute and chronic effects of hypothalamic lesions on feeding may involve different mechanisms (Harrell & Remley, 1973), the implications of the present findings on feeding and gastric pathology should be limited to the demonstration that stomach ulceration can occur concomitantly with aphagia or hyperphagia, whether these acute feeding disturbances are caused by stimulation, destruction of tissue, or any other mechanism.…”

“…On the other hand, ulcers induced by both medial and lateral hypothalamic lesions did resemble ulcers induced by various experimental "stress" procedures in terms of location in the stomach and general appearance (Gheorghiu, 1975;Pare & Livingston, 1970). There have been suggestions that some of the acute effects of hypothalamic lesions, for example, hypertension (Reis et aI., 1976), hyperactivity (Reis et aI., 1976;Whishaw & Robinson, 1974), and the hyperphagia seen after VMH lesions (Harrell & Remley, 1973), may be due to irritative effects of anodal iondepositing electrolytic lesions. In other words, these effects might be due to stimulation rather than destruction of brain tissue.…”

“…The observation that medial hypothalamic placements associated with gastric pathology induced voracious eating and drinking starting soon after recovery from anesthesia, while lateral animals consistently refused to eat and drink at that time, constitutes additional evidence against the possibility that LH feeding deficits result from the concomitant gastric pathology. However, since feeding has a protective effect against some types of ulcers (Cosen & Mazure, 1975;Mikhail, Gabriel, & Glavin, 1977), it might be argued that perhaps the immediate lesioninduced feeding of VMH rats (Harrell & Remley, 1973) usually prevents ulcer formation, while LH rats become chronically aphagic because ulceration is allowed to develop before normal postlesion feeding would resume. We have observed, however, that VMH rats with no postoperative food will readily consume food offered to them 24 h after the lesion, at a time when ulcers are already fully formed.…”

“…Hypothalamic lesions can induce a number of autonomic and behavioral effects, including motor hyperactivity (Harrell & Remley, 1973;Maire & Patton, 1954;McGinty, 1969;Whishaw & Robinson, 1974), alterations in feeding behavior (Harrell & Remley, 1973; Schallert, Whishaw, & Flannigan, 1977), gastric ulceration (Anderson & Haymaker, 1974; Cushing, 1932;French, Porter, von Amerongen, & Raney, 1952; Hoff & Sheehan, 1935; Long, Leonard, & French, 1962;Watts & Fulton, 1935), and changes in pulmonary and cardiovascular functions (Maire & Patton, 1954; Reis, Gauthier, & Nathan, 1976). There is no generally accepted view of the relations among these various changes, not all of which necessarily result from the same hypothalamic lesion placements.…”

“…While lateral hypothalamic lesions can cause feeding deficits and stomach pathology within 24 h of the lesion (Schallert et aI., 1977), the time course for the development of ulceration after medial hypothalamic lesions, which can induce eating early in the postoperative period (Harrell & Remley, 1973), has not been determined.…”