Further studies on salt appetite following lateral hypothalamic lesions: Effects of preoperative alimentary experiences.

Lateral hypothalamic lesions impair salt appetite, but rats with lesions show enhanced saline ingestion following natrorexigenic treatments if given preoperative salt drive experiences. In the present study, with 118 male Holtzman rats, the preoperative drive to ingest salt (without the consummatory experience of saline ingestion) was found to be both necessary and sufficient for this effect. Exposure to saline, or the treatments of water deprivation or insulin-induced feeding, were not protective when given preoperatively. (27 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Two types of aphagia and two types of sensorimotor impairment after lateral hypothalamic lesions: Observations in normal weight, dieted, and fattened rats.

Examined reactions to food and to tactile stimuli in 2 experiments with 64 male Sprague-Dawley and Long-Evans rats whose body weights were normal, reduced by restricted feeding (dieted), or raised by having access to palatable foods (fattened) prior to receiving bilateral lesions in the lateral hypothalamic (LH) area. Postoperative aphagia and sensorimotor impairments were less prolonged than normal in the dieted Ss and more prolonged than normal in the fattened Ss. The LH lesions produced a transient hyperthermia that was attenuated by dieting and facilitated by fattening. Depending importantly upon lesion placement, there appeared to be at least 2 types of aphagia and 2 types of sensorimotor impairment. Ss with more posterior LH lesions displayed a passive kind of aphagia and sensory neglect. Animals with more anterior LH lesions displayed an active kind of aphagia and sensory rejection. Animals with intermediately placed lesions showed symptoms common to passive and active aphagia and to sensory neglect and sensory rejection. The effects of preoperative weight manipulation on the specific types of aphagia and sensorimotor impairments are discussed. (2 p ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Dissociation of gustatory and weight regulatory responses to quinine following lateral hypothalamic lesions.

In a 2-phase experiment, consummatory (Phase 1) and body weight regulation (Phase 2) responses to quinine adulteration of a wet mash diet were measured in 16 Holtzman male albino rats recovered from bilateral lateral hypothalamic lesions (LH) and in 18 unoperated control rats (C). In Phase 1, all were fed wet mash adulterated with increasing concentrations of quinine sulfate every other day and fed unadulterated wet mash on the alternate days. Group LH consumed a significantly lower proportion of quinine-adulterated wet mash relative to unadulterated wet mash, displaying a steeper concentration-response function and a lower rejection threshold than did Group C. In Phase 2, Groups LH and C were maintained exclusively on quinine-adulterated mash for 20 days. This procedure caused equivalent weight loss in the 2 groups. Therefore, an apparent exaggerated aversion to quinine-adulterated food does not appear to contribute abnormally to the weight regulation exhibited by rats with lateral hypothalamic damage. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lateral hypothalamic lesions and vagotomy on meal patterns in rats.

Studied meal patterns with liquid diets in 4 female Carworth CFE albino rats with lateral hypothalamic (LH) lesions and in 4 Ss with sham lesions, both before and after vagotomy. LH Ss reduced total intake following lesions but showed no differences from controls after vagotomy on measures of total daily intake, mean meal size, and frequency of feeding. Identical frequency distributions of meal sizes and intermeal interval durations were found in LH and control Ss after vagotomy. However, although sham-lesioned Ss showed significant positive correlations between meal size and subsequent intermeal-interval durations in all phases of the experiment, the LH Ss showed no such correlation following vagotomy. Thus, indices of microregulatory controls may be more sensitive in indicating feeding deficits. (25 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

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

Investigated the role of the vagus in the lateral hypothalamic (LH) syndrome to body weight loss in 80 male Sprague-Dawley albino rats. Ss were divided into 4 groups: (a) Ss with bilateral LH lesions that were subsequently given a bilateral subdiaphragmatic vagotomy, (b) LH Ss that received a control vagotomy operation, (c) nonlesion Ss that were given a subdiaphragmatic vagotomy, and (d) nonlesion Ss 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. Gastric contents after a 24-hr fast were greater in vagotomized than in nonvagotomized Ss. These data are discussed in relation to the role of the vagus in maintaining body weight levels and in relation to the changes in gastric functioning after LH lesions and vagotomy. (42 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Restricted feeding and its effects on aphagia and ingestion-related disorders following lateral hypothalamic damage

Previous studies have shown that lateral hypothalamic (LH) damage produces aphagia, gastric pathology, hyperthermia, and sensorimotor dysfunctions. Furthermore, preoperative dieting has been reported to shorten the period of aphagia, reduce the incidence of gastric pathology, attenuate the hyperthermia, and facilitate recovery of certain sensorimotor dysfunctions following LH lesions in rats. The present study compared the effects of dieting and two additional restricted feeding regimens (meal feeding alone or in combination with a high-carbohydrate supplement) which produced different body weight functions on several disorders induced by LH lesions. Restricted feeding (i.e., dieting and meal feeding), which resulted in approximately at 5% to 25% drop in body weight prior to LH lesions, similarly shortened the period of postoperative aphagia, reduced the incidence of gastric pathology, prevented the hyperthermia, and facilitated recovery of responsivity to tactile stimulation; however, other sensorimotor dysfunctions were relatively unaffected. Because the initial reinstatement of eating occurred at different body weight levels and in the presence of obvious sensorimotor abnormalities, it is unlikely that either body or sensorimotor dysfunctions per se are critical factors in determining the period of aphagia. The results are more consistent with the view that metabolic disorders that are attenuated by restricted feeding significantly contribute to the ingestive deficits of LH-damaged rats.     

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 drink water simply to facilitate the consumption of dry food. However, the present results from adult Sprague-Dawley albino rats indicate that these Ss 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 Ss 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, suggest a new interpretation of the lateral hypothalamic syndrome. (2 p ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Recovery of salt appetite after lateral hypothalamic lesions: Effects of preoperative salt drive and salt intake experiences.

75 male mongrel rats were divided into lateral hypothalamic (LH)-lesion or intact control groups. The LH-lesion groups (1) had no salt experience prior to induction of lesions, (2) had experience of both salt drive and saline intake, (3) had salt drive but no saline experience, or (4) had no salt drive experience but saline intake experience. Results confirm earlier findings that preoperative salt experiences can protect the rat against the usual deficit in regulatory salt intake that follows such lesions. However, results suggest that there may be no specific feature of the preoperative salt experience that is critical for the protective effect, since both salt drive experience without concomitant salt intake experience and salt intake experience without concomitant salt drive experience were effective. (8 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lateral hypothalamic lesions on placentophagia in virgin, primiparous, and multiparous rats.

Produced lesions of the lateral hypothalamus (LH) in 25 pregnant and 25 nonpregnant Sprague-Dawley rats through chronically implanted electrodes to investigate the effect of LH damage on placentophagia. Other variables investigated were prior parturitional experience and stimulus properties of the placenta. Lesions were produced under either anesthesia 24 hr prior to parturition in pregnant Ss and 24 hr prior to placenta presentation in nonpregnant Ss. Lesions produced aphagia to a liquid diet. Pregnancy was not a significant variable in the initiation of placentophagia, but prior parturitional experience was critical. Virgin and primiparous Ss did not exhibit placentophagia following LH damage, but multiparous Ss would eat placenta whenever the opportunity arose, independently of LH damage and pregnancy. (18 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lateral hypothalamic lesions on food intake of rats during exposure to cold.

Two experiments investigated the feeding behavior of 41 male Sprague-Dawley rats with lateral hypothalamic (LH) lesions and 13 Ss with chemical lesions of central dopaminergic neurons. LH damage impaired both physiological and behavioral responses of Ss during exposure to a 5°C environment. The LH-lesioned Ss usually did not conserve heat in the cold as well as did controls (n?=?13), nor did they always increase their caloric intake to meet their energy needs. However, when given sucrose solution to drink instead of water, LH-lesioned Ss increased their ingestion of chow in response to cold exposure. It is likely that the elevated consumption of palatable fluid served to relieve dehydration and thereby removed its constraints on eating, thus permitting hyperphagia to occur. In contrast to these results, Ss with large dopamine-depleting brain lesions, produced by intraventricular 6-hydroxydopamine treatments, always increased food intake when exposed to cold stress and demonstrated no apparent problems in peripheral vasoconstriction. Thus, it is unlikely that striatal dopamine depletions account for either the impaired feeding response or the inadequate heat conservation of rats with lateral hypothalamic lesions during cold stress. (33 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Adrenocortical response to hypertonic saline in rats with lateral hypothalamic lesions.

Used plasma corticosterone levels to assess the response to stress induced by ip injections of hypertonic saline in 27 male albino Harlan-Sprague rats with lateral hypothalamic (LH) or sham lesions. Ss with LH lesions displayed a corticosterone response equal to that of normal Ss under basal conditions, after control injections of isotonic saline, and 20 min after injection of hypertonic saline (1.5 M, 1.0 ml/100 g of body weight). The corticosterone response of Ss with LH lesions, however, was significantly less than that of normal Ss 90 min after injection of hypertonic saline when no water was available. With access to water, normal Ss displayed substantial drinking (14.5 ml/90 min), which resulted in a reduction in plasma corticosterone concentrations to a level observed after a control injection of isotonic saline, but the little water ingested by Ss with LH lesions (2.5 ml) had no effect on the pituitary-adrenal system. It is concluded that the failure of Ss with LH lesions to drink following a hydrational challenge is not the result of an exaggerated response to stress. (17 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Further analysis of sensory inattention following lateral hypothalamic damage in rats.

Reports results of 2 experiments with a total of 14 Sprague-Dawley albino, 17 Charles-River albino, and 8 Long-Evans hooded rats. Ss with lateral hypothalamic damage had severe impairments in orienting to sensory stimuli and in using their limbs. When damage was unilateral, these deficits occurred only on the side contralateral to the lesion. Bilateral damage caused bilateral sensorimotor impairments which were involved in the early postoperative deficits in feeding and killing. Sensorimotor capacities recovered gradually and in a predictable fashion. Several aspects of the sequence of recovery were parallel to the ontogeny of sensorimotor capacities. Finally, these impairments seemed to be associated with damage to an area in the ventrolateral hypothalamus-subcapsular area, where pallidohypothalamic and amygdalohypothalamic fibers reportedly pass. (61 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Adipsia produced by lateral hypothalamic lesions: Facilitation of recovery by preoperative restriction of water intake.

Conducted 2 experiments in which 44 male Sprague-Dawley rats were adapted to various food and water schedules before being lesioned and tested for adaptation behavior. Following lesions in the lateral hypothalamic area, Ss failed to drink water for several postoperative days. This dysfunction was attenuated or prevented completely in Ss subjected preoperatively to a restricted daily watering regimen. Postoperative drinking was vigorous and was not feeding-associated. Reactivity to sensory stimuli was enhanced both pre- and postoperatively, particularly to stimuli associated with water. Larger lesions produced longer periods of adipsia that were resistant to the preoperative regimen. It is suggested that restricted watering may exert its protective action via several central and peripheral mechanisms, but a behavioral/physiological conditioning hypothesis is emphasized. (71 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Gastric pathology and feeding deficits induced by hypothalamic damage in rats: Effects of lesion type, size, and placement.

In a study with 146 male Sprague-Dawley rats, 3 doses each of cathodal or anodal direct current were delivered bilaterally to coagulate lateral hypothalamic tissue. Increases in hypothalamic tissue damage were associated with more instances of aphagia, greater amounts of glandular, but not rumenal, gastric pathology (GP), and greater weight loss. Both anodal and cathodal lesions produced aphagia and similar amounts of GP, but anodal lesions also facilitated weight loss independently of tissue damage. It is suggested that extensive chromatolysis surrounding anodal lesion cavities may be related to the postoperative effects. When anodal electrolytic lesions or cortical suction ablations were used to vary the location of neural damage, eating of dry food in the presence of high GP was observed in Ss with lesions ventral and medial to an area in the dorsolateral hypothalamus that was associated with aphagia. When aphagia was accompanied by severe GP, the brain lesions typically encroached extensively on more ventromedial areas. Moreover, aphagia sometimes was observed with only negligible GP. It is suggested that GP is not primary to the expression of the aphagia that follows lateral hypothalamic damage. (44 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Weight regulation with palatable food and liquids in rats with lateral hypothalamic lesions.

Maintained 25 female Carworth CFE albino rats with 4- or 7-sec 1-ma bilateral lesions of the lateral hypothalamus (LH) for 87 days on a high-fat diet and a sequence of fluids (water, 6% sucrose, and 1 or .2% saccharin). Lesioned Ss reached a greater weight than 9 sham-lesioned Ss offered the same diet and fluids, and maintained greater weight regardless of the fluid offered. These data do not support the hypothesis that LH lesions lower the set point for weight. Rather, the finickiness of LH Ss results in smaller intake of unpalatable foods and water which, in turn, results in stablization of weight below that of controls. If sufficiently hydrated, LH Ss eat greater quantities of highly palatable foods than do controls, resulting in greater body weight. (24 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

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 (LH) area do not show the normal feeding response to 2-deoxyglucose or drinking response to polyethylene glycol. The present work found 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 male albino Sprague-Dawley rats with LH lesions that were similar to those observed after 2-deoxyglucose. Results suggest that the residual feeding and drinking deficits of Ss with LH lesions after apparent recovery of function do not reflect specific loss of putative gluco- and volume-regulatory contributions to ingestive behavior. Instead, they indicate continued impairments in nonspecific activational components of motivation that normally are mediated, in part, by central dopaminergic neurons. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

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

Eight sighted male albino 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. Nine intact controls were also studied. Following these injections, drinking was observed only during the nighttime. After morning injections Ss frequently waited until nightfall before drinking, whereas Ss 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 6 blind lesioned Ss suggest that these effects were due to an endogenous circadian rhythm. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of ventromedial hypothalamic lesions on hunger-motivated behavior in rats.

Previous studies show that lesions of the ventromedial hypothalamus (VMH) paradoxically increase food intake and decrease hunger motivation in the rat. In a series of experiments designed to examine this paradox, independent groups of VMH-lesioned, female hooded rats (N = 48) were tested on a VI schedule or were run in a straight alley to a food reward. Rate of food ingestion was also measured for all Ss. Performance of the VMH and control groups was compared at identical deprivation conditions defined in terms of preoperative base-line weights (80, 90, 100, and 110%). All test measures showed a significantly higher level of performance for VMH-lesioned Ss at the least severe deprivation conditions. Results suggest that the previously reported VMH paradox originated, in part, from inappropriate testing procedures and between-group comparisons. (20 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of preoperative training on food-motivated behavior of hypothalamic hyperphagic rats.

Conducted an experiment in which 35 female Holtzman albino rats with lesions in the ventromedial hypothalamic area performed significantly more poorly than 18 normal controls on a food-motivated task. This result was obtained, however, only if Ss were not preoperatively trained on the task. Ss trained preoperatively did not show any deficit and their performance was comparable to that of normal Ss. Findings suggest that the performance of hypothalamic hyperphagic rats on appetitively motivated tasks is a function of training and testing conditions rather than lower food motivation. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

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

Investigated the development of feeding patterns in weanling rats and in rats with lateral hypothalamic lesions. 2 experiments were conducted with a total of 39 male albino Sprague-Dawley rats. 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) such that by 30-35 days of age a full adult pattern was observed. Ss recovering from lateral hypothalamic lesions, for a brief period, also demonstrated a preprandial intake pattern. The postprandial relationship was abolished by the lesion. Results suggest that the development of adult meal patterning results from maturation of lateral hypothalamic mechanisms governing meal initiation. (40 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)