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.     

Gastric pathology and aphagia following lateral hypothalamic lesions in rats: effects of preoperative weight reduction.

The body weights of male albino rats were reduced gradually to 80% of normal body weight by resricting food intake (dieting), and then the rats were given lateral hypothalamic (LH) lesions. Compared with rats of normal body weight sustaining similar brain lesions, the dieted group displayed a shorter period of postoperative aphagia and less gastric pathology. In a second experiment, a group of rats was reduced to 80% of normal body weight by withholding all food (fasting) and then given LH lesions. Compared with dieted rats sustaining similar brain damage, the fasted group displayed a longer period of post operative aphagia and greater gastric pathology. Since the duration of aphagia could be shortened or lengthened by simple manipulations of preoperative body weight, the adequacy of sensorimotor or motivational hypotheses to account for aphagia is questioned. The results are more consistent with the suggestion that gastric abnormalities produced by LH lesions inhibit eating.     

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.     

Acute homeostatic imbalances reinstate sensorimotor dysfunctions in rats with lateral hypothalamic lesions

It has previously been demonstrated that rats recovered from aphagia and adipsia after large bilateral electrolytic lesions of the lateral hypothalamic area do not show the normal feeding response to 2-deoxyglucose or drinking response to polyethylene glyol. The present work reveals that such homeostatic imbalances reinstate the profound sensorimotor impairments that are seen in the immediate postoperative period but abate in parallel with the gradual recovery of ingestive behaviors. Administration of alpha-methyltyrosine or spiroperidol produced sensory and motor dysfunctions in rats with lateral hypothalamic lesions that were similar to those observed after 2-deoxyglucose. These results suggest that the residual feeding and drinking deficits of rats with lateral hypothalamic lesions after apparent recovery of function do not reflect specific loss of putative gluco- and volume-regulatory contributions to ingestive behavior. Instead, they may indicate continued impairments in nonspecific activational components of motivation that normally are mediated, in part, by central dopaminergic neurons.     

Circadian rhythms and partial recovery of regulatory drinking in rats after lateral hypothalamic lesions.

Rats that had recovered spontaneous ingestive behavior after lesions of the lateral hypothalamus were challenged with acute injections of hypertonic NaCl administered at different times during the day/night cycle. Following these injections, drinking was observed only during the nighttime. After morning injections the rats frequently waited until nightfall before drinking, whereas animals injected at night showed much shorter delays in the behavioral response; a similar nocturnal predominance of drinking was seen after food deprivation and in the ad-lib situation. Studies in blinded animals suggested that these effects were due to an endogenous circadian rhythm.     

Body weight and gastric acid secretion in rats with subdiaphragmatic vagotomy and lateral hypothalamic lesions

In an experiment to investigate the role of the vagus in the lateral hypothalamic (LH) syndrome of body weight loss, male albino rats were divided into four groups: (a) animals with bilateral LH lesions that were subsequently given a bilateral subdiaphragmatic vagotomy, (b) LH animals that received a control vagotomy operation, (c) nonlesion animals that were given a subdiaphragmatic vagotomy operation, (c) nonlesion animals that were given a subdiaphragmatic vagotomy, and (d) nonlesion animals that received a control vagotomy operation. Both LH lesions and vagotomy reduced body weight levels, though the effects differed in terms of the length of time required to reach initial maximal loss, the time required to reach chronic levels of maintenance, and the severity of body weight reduction. Fasting gastric acid secretion was lowered by LH lesions, and the extent of this reduction was positively correlated with the reduction in body weight. Finally, gastric contents after a 24-hr fast were greater in vagotomized rats than in nonvagotomized animals. These data are discussed in relation to the changes in gastric functioning after LH lesions and vagotomy.     

Ontogeny of meal patterning in rats and its recapitulation during recovery from lateral hypothalamic lesions.

The development of feeding patterns was investigated in weanling rats and in rats with lateral hypothalamic lesions. From 16 to 25 days of age, the weanlings demonstrated a preprandial intake pattern, i.e., a positive correlation between meal size and time since the preceding meal. This subsequently declined while the postprandial relationship (correlation with time until subsequent meal) began to emerge such that by 30-35 days of age a full adult pattern was observed. Rats recovering from lateral hypothalamic lesions, for a brief period, also demonstrated a preprandial intake pattern. The postprandial relationship was abolished by the lesions. These results suggest that the development of adult meal patterning results from maturation of lateral hypothalamic mechanisms governing meal initiation.