The relationship of energy expenditure and spontaneous activity to the aphagia of rats with lesions in the lateral hypothalamus

Abstract

SUMMARY1. Lesions in the lateral hypothalamus of rats always produced an immediate increase in total energy expenditure. The increase was maintained for 24 hr or longer only in rats that became and remained aphagic. Rats that showed no recovery from the aphagia and were maintained by tube feeding showed a second, larger increase in metabolic rate after about 7 days.2. The increase in total energy expenditure was associated, initially, with almost continuous motor activity. With continued aphagia an abnormally differentiated pattern of activity appeared at the same time as the second increase in metabolic rate, and the compartment of energy attributable to activity remained high (34 % as compared with 23 % in normal rats). These changes were accompanied by a recovery of an instrumental response for food (lever pressing), of interest in offered foods and of grooming activity.3. Metabolic abnormality not attributable to activity was indicated by increased creatinine excretion of aphagic but not of hypophagic rats.4. Rats that recovered spontaneous feeding after aphagia returned towards a normal differentiated pattern of activity, with bursts of activity separated by periods of rest, but showed residual abnormality in creatinine excretion.5. The intimate association between increase of energy expenditure, abnormality of motor activity and the aphagia produced by lateral hypothalamic lesions is consistent with the hypothesis that motor incoordination or disorganization is a cause of the aphagia.

Lateral hypothalamic lesions and norepinephrine turnover in rats.

“…Opsahl (41) (11)(12)(13)(14) observed in the acute (12)(13)(14) and chronic (11) phase following such lesions, as well as the rise in core temperature (15). It might also account for the gastric ulcerations (9, 10) and microhemorrhagic gastritis observed in our LH-lesioned rats.…”

“…Four rats were used at each time point to obtain the turnover data. (6,29) associated with an increase in metabolic rate (12)(13)(14) and erosive lesions of the gastric mucosa (9, 10). These gastric erosions are similar to the gastric ulcers produced in restrained rats (30).…”

“…Recent studies have demonstrated that lesions in the lateral hypothalamus are associated with gastric ulcers (9,10). In addition, there is an increase in overall metabolism, which persists for at least 3 mo after LH lesions (11) and is manifested as an increase in oxygen consumption within hours after the LH lesion (12)(13)(14). There is also a persistent elevation in core temperature following LH lesions (15).…”

Facilitation of survival following lateral hypothalamic damage by prior food and water deprivation

“…This result is inconsistent with the weight regulation model oi Powley & Keesey (1970) if reduced catabolism and facilitated recovery are functions of the same process. Although spontaneous eating and drinking with recovery did not occur in the present experiment, a direct relationship 164 between enhancement of recovery and reduction of catabolism has previously been implicated (Morrison, 1968).…”

“…The present experiment was designed to further investigate the effect of preoperative starvation on early pos topera tive changes in lateral hypothalamic rats. Lateral hypothalamic lesions enhance catabolic processes (Morrison, 1968), resulting in quicker death than would follow from eontinuous food and water deprivation of normal rats. On a si mplistie basis of enhanced postoperative stress and fatigue, it would be expected that food and water deprivation prior to lesioning the lateral hypothalamus would impair postoperative survival if such rats were not given special postoperative eare (Le., tube feeding, very palatable foods, etc.).…”