Drinking by rats after lateral hypothalamic lesions: a new look at the lateral hypothalamic syndrome.

Rats that have recovered from aphagia and adipsia following lateral hypothalamic lesions are believed to be incapable of experiencing thirst and to drink water simply to facilitate the consumption of dry food. However, the present results indicate that these animals will drink in response to dehydration of the intracellular or intravascular fluid compartments and to hyperangiotensinemia, if testing continues beyond a few hours. Comparable effects also were obtained in rats with mesencephalic brain damage, which appeared to destroy portions of the substantia nigra and the ascending nigrostriatal dopaminergic projections. These findings, when placed in the context of a recent neurochemical model for recovery of function, provide the basis for a new interpretation of the lateral hypothalamic syndrome.     

Role of activation and sensory stimuli in recovery from lateral hypothalamic damage in the cat

The early stages of recovery from lateral hypothalamic lesions were analyzed in 30 adult cats. In addition to aphagia and adipsia, neurological examination revealed deficits suggestive of deficient endogenous arousal, including somnolence, catalepsy, akinesia, and sensory neglect. Manipulations (tail pinch and injection of amphetamine) that counteracted these deficits also restored feeding. During recovery from aphagia, feeding gradually became activated by sensory stimuli (sight, feel, and smell) associated with food. These data suggest that activation is an important component in the control of normal feeding.     

Gastric mucosal damage induced by lateral hypothalamic lesions in female rats: influence of age and ovariectomy

Male rats given lateral hypothalamic (LH) lesions exhibit an acute increase in gastric acid secretion and develop erosions of the glandular portion of the stomach within 24 h. Since this process has been examined predominantly in male rats, the present experiments were devised to study the effects of LH lesions on the gastric mucosa of female rats. In Experiment 1, 1-year-old Sprague-Dawley female rats given LH lesions exhibited erosions in the rumenal portion of the stomach, a pattern unlike that found in both young and old male rats. Although the glandular mucosa lacked evidence of gross defects, the mucosa appeared blanched and covered with a mucus-like secretion. Experiment 2 demonstrated that, like male rats, LH lesions produced gastric hypersecretion in 1-year-old females. The results of the first two experiments indicate that the dissimilar patterns of gastric mucosal injury between males and older females cannot be accounted for on the basis of differences in gastric acid secretion. Experiment 3 demonstrated that, unlike older females but like males, 4-month-old female rats given LH lesions developed gastric erosions in the glandular mucosa only. Additionally, ovariectomy had no significant effect in altering the extent of gastric pathology. Taken together, these results suggests that (1) age and gender are important variables in neurogenic gastric mucosal injury, (2) differences in the type of gastric ulceration cannot be accounted for by differences in acid secretion, (3) ovarian hormones do not appear to play a significant role in gastric ulceration following brain damage.     

Non-interaction of ventromedial and lateral hypothalamic mechanisms in the regulation of feeding and hoarding behaviour in the rat

Lesions of the hypothalamic ventromedial nucleus (VMN) led to an immediate increase in food intake but not to any increase in hoarding activity. Later, when subjects were very obese, they failed to hoard even in response to a 16-hr. deprivation schedule, although this schedule did produce hoarding if body weights were held at, or were brought down to, preoperative levels. These results indicate that the lateral hypothalamic mechanism responsible for hoarding and feeding responds to long-term nutritional factors, and that it is not directly affected by the short-term satiety mechanisms in the VMN. These findings support the hypothesis (a) that even “non-physiological” activities (e.g. hoarding, exploration) are motivated by physiological needs, and (b) that the reason these activities do not ordinarily covary with physiological drives is that, unlike the physiological drives, they are not subject to inhibition by the hypothalamic satiety mechanisms.