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

Conducted 2 experiments with a total of 105 male albino rats. In Exp I, body weights of Ss were reduced gradually to 80% of normal weight by restricting food intake (dieting), and then Ss were given lateral hypothalamic (LH) lesions. Compared with Ss of normal body weight sustaining similar brain lesions, the dieted group displayed a shorter period of postoperative aphagia and less gastric pathology. In Exp II, a group of Ss was reduced to 80% of normal body weight by withholding all food (fasting) and then given LH lesions. Compared with dieted Ss sustaining similar brain damage, the fasted group displayed a longer period of postoperative 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. Results are more consistent with the suggestion that gastric abnormalities produced by LH lesions inhibit eating. (60 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Decreased metabolic rates contingent upon lateral hypothalamic lesion-induced body weight losses in male rats.

In 3 experiments with 146 male Charles River rats, Ss that had reduced body weights following small lateral hypothalamic (LH) lesions also had lower fasting heat production (FHP, equivalent to basal metabolic rate). The decreased FHPs were not a secondary consequence of reduced body weight, since Ss whose body weights had been chronically reduced by restricting their water intake did not show a reduction in FHP. Ss with lesions were adipsic and aphagic only for a brief period and had none of the permanent deficits associated with the LH syndrome. They drank water when it was presented alone, they were not prandial drinkers, and they ate following systemic hypoglycemia. The FHPs of Ss with LH lesions were elevated immediately postsurgery, but dropped below normal after about 1 wk. These decreased FHPs were not the result of any change in the Ss activity levels. The thyroids of Ss with LH lesions were smaller and their blood levels of thyroxine were lower than those of the sham Ss. In addition, goiters resulting from the ingestion of a diet containing .015% propylthiouracil were significantly smaller in Ss with LH lesions than in sham Ss. Complete thyroidectomy of normals resulted in weight curves identical to those Ss with the largest LH lesions and lowest FHPs. (28 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Vagotomy facilitates extinction of conditioned taste aversions in rats.

Results from 3 experiments indicate that severing the subdiaphragmatic vagus in male Sprague-Dawley rats increased the rate of extinction of learned taste aversions. In Exp I, when the illness-inducing agent was the blood-borne toxin apomorphine, vagotomized Ss tended to consume more saccharin than controls during repeated extinction tests. In Exp II, vagotomy disrupted retention and increased extinction of a preoperatively acquired saccharin aversion. Disruptions were found when the taste aversion was induced by copper sulfate, a local gastric irritant, or apomorphine. Exp III demonstrated that vagotomy did not affect retention or extinction of a shock-induced conditioned emotional response to noise. It is concluded that integrity of the vagus is not necessary for acquisition of a learned taste aversion when a blood-borne toxin is used as the illness-inducing agent. However, the vagus apparently mediates an integral portion of the CR following taste–illness acquisition. (24 ref) (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)     

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)     

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)     

Vagotomy blocks hypothalamic hyperphagia in rats on a chow diet and sucrose solution, but not on a palatable mixed diet.

Adult female Sprague-Dawley rats were given ventromedial hypothalamic parasagittal knife cuts (VMH treatment) or control surgery (Con treatment), followed 10 days later by subdiaphragmatic vagotomy (Vag treatment) or sham vagotomy (Sham treatment). The hyperphagia and obesity produced by the VMH cuts to Ss on a chow diet was completely blocked by vagotomy (VMH-Vag group). Vag also inhibited the VMH Ss' overconsumption of a 20% sucrose solution during 1-hr/day and 24-hr/day tests, which contrasts with the effects of atropine treatment. However, when offered a selection of palatable foods (cookies, sweet milk, high-fat ration) in addition to chow, VMH-Vag Ss overate and gained considerably more weight than did the Con-Vag or the Con-Sham Ss. Con-Vag Ss, on the other hand, gained less weight than Con-Sham Ss on the palatable diet. Results indicate that intact subdiaphragmatic vagi are not essential for the expression of VMH hyperphagia and finickiness, and they therefore question the role of vagally mediated cephalic responses in the hypothalamic hyperphagia syndrome. On the other hand, results indicate that in brain-intact animals Vag suppresses the development of diet-induced obesity. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Abdominal vagotomy disrupts food-related drinking in the rat.

In 2 experiments with a total of 41 Sprague-Dawley albino rats, Ss with complete subdiaphragmatic bilateral transection of the abdominal vagus (Vgx-C) showed disordered food-related drinking when drinking water in temporal association with a meal of dry food after 5-hr food deprivation and when drinking water in association with a liquid meal after 24-hr food deprivation. The Vgx-C Ss drank after significantly longer latencies and drank significantly less water in 1 hr than did sham-vagotomized (Sham) Ss after eating the same size meal (solid or liquid). Ss with incomplete vagal transection (Vgx-I) ate and drank like Shams. Water intake of Sham and Vgx-I Ss correlated positively with the meal size of solid food, but the water intake of Vgx-C Ss did not. The failure of Vgx-C Ss to drink water normally when food was ingested was not due to failure of a food stimulus to reach the intestine, because Vgx-C and Sham Ss emptied equivalent volumes of liquid food from the stomach into the intestine within 10 min of food entering the stomach. Results indicate that the abdominal vagus is an important neurological substrate for food-related drinking in the rat. (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)     

Somnogenic and pyrogenic effects of interleukin-1beta and lipopolysaccharide in intact and vagotomized rats

The vagus nerve appears to serve a role in mediating peripheral immunologic influences on CNS processes. Previous work demonstrates that subdiaphragmatic vagotomy prevents or attenuates many of the behavioral and physiological responses to exogenous interleukin-1 (IL-1) or lipopolysaccharide (LPS). We determined whether the somnogenic effects of IL-1 and LPS were altered in vagotomized rats, and whether the effects of vagotomy on IL-1- and LPS-induced alterations in sleep would vary as a function of circadian phase. The data indicate that vagotomy does not influence the normal circadian patterns of sleep and wakefulness in untreated rats, or modify the pyrogenic or somnogenic effects of intracerebroventricular administration of IL-1. However, in unchallenged animals vagotomy reduces basal brain temperatures, increases delta wave amplitudes during slow-wave sleep (SWS), and induces a reduced rate of weight gain, gastric distension, and adrenal hypoplasia. Vagotomy attenuates the febrile effects of IL-1 during both light and dark phases, attenuated IL-1-induced sleep enhancement during the dark phase, and attenuated IL-1-induced increases in delta wave amplitudes within SWS during the light period. In LPS-treated rats, vagotomy attenuates the febrile and SWS responses to LPS after administration at light onset, but not after administration at dark onset. These results indicate that subdiaphragmatic vagotomy attenuates several of the somnogenic and pyrogenic effects of IL-1beta and LPS, although the effectiveness of the vagal transection in modulating these responses is influenced by circadian factors.     

Vagotomy Blocks Hypothalamic Hyperphasia in Rats on a Chow Diet and Sucrose Solution, but Not on a Palatable Mixed Diet: Correction.

Reports an error in the original article by A. Sclafani, P. Aravich and M. Landman (Journal of Comparative and Physiological Psychology, 1981, Vol. 95, No. 5, 720-734). Table 3 contains several errors in the mean and standard error values for the second and third groups. The correct table is provided. (The following abstract of this article originally appeared in record 1982-09338-001): Adult female Sprague-Dawley rats were given ventromedial hypothalamic parasagittal knife cuts (VMH treatment) or control surgery (Con treatment), followed 10 days later by subdiaphragmatic vagotomy (Vag treatment) or sham vagotomy (Sham treatment). The hyperphagia and obesity produced by the VMH cuts to Ss on a chow diet was completely blocked by vagotomy (VMH-Vag group). Vag also inhibited the VMH Ss' overconsumption of a 20% sucrose solution during 1-hr/day and 24-hr/day tests, which contrasts with the effects of atropine treatment. However, when offered a selection of palatable foods (cookies, sweet milk, high-fat ration) in addition to chow, VMH-Vag Ss overate and gained considerably more weight than did the Con-Vag or the Con-Sham Ss. Con-Vag Ss, on the other hand, gained less weight than Con-Sham Ss on the palatable diet. Results indicate that intact subdiaphragmatic vagi are not essential for the expression of VMH hyperphagia and finickiness, and they therefore question the role of vagally mediated cephalic responses in the hypothalamic hyperphagia syndrome. On the other hand, results indicate that in brain-intact animals Vag suppresses the development of diet-induced obesity. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Influence of sympathectomy on the lateral hypothalamic lesion syndrome.

Two experiments with male Long-Evans rats examined sympathetic involvement in the lateral hypothalamic (LH) lesion syndrome. Ss were surgically or chemically sympathectomized and then given LH lesions. At 24 hrs postlesion, lesion-induced hyperglycemia but not hyperthermia was attenuated by splanchnicectomy and celiac ganglionectomy. Hyperthermia but not hyperglycemia was attenuated by adrenal demedullation, adrenalectomy, and daily neonatal guanethidine (50 mg/kg) treatment. Guanethidine-sympathectomized Ss also displayed lower basal temperatures, more perilesion chromatolysis, and more severe external symptoms than controls. No form of sympathectomy affected lesion-induced gastric pathology, plasma gastrin concentrations, or body weight loss, nor did any sympathectomy influence the recovery of ingestive behavior, daily food intake, the feeding response to 2-deoxy-dextro-glucose, or body weight maintenance in recovered LH-lesioned Ss. Results suggest that sympathetic hyperactivity contributed to some aspects of the acute LH syndrome: Hyperglycemia resulted from sympathetic outflow to the abdomen, whereas hyperthermia was determined by circulating catecholamines and extra-abdominal sympathetic innervation. Findings fail to support the hypothesis that chronic increases in sympathetic tone are responsible for the reduced food intake and body weight of the LH-lesioned Ss. (47 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.     

Sham feeding in rats after ventromedial hypothalamic lesions and vagotomy.

Two studies examined sham feeding in female Sprague-Dawley rats with ventromedial hypothalamic (VMH) lesions with or without abdominal vagotomy. In Exp I, intact Ss consumed more than twice as much sweet milk during 1-hr tests of sham feeding as they did when feeding normally. Ss with VMH lesions showed exaggerated sham feeding, which was elevated almost four-fold over their already high normal feeding baseline. In Exp II, vagotomy substantially reduced sham feeding in Ss with VMH lesions. After vagotomy, VMH Ss sham fed half as much as nonvagotomized VMH Ss. Vagotomy did not, however, reduce sham feeding to control levels. Results are consistent with the hypothesis that VMH hyperphagia arise from exaggeration of orosensory responsiveness, which is, in part, a consequence of perturbed vagal function. (40 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Multiple knife cuts between the medial and lateral hypothalamus in the rat: A reevaluation of hypothalamic feeding circuitry.

In 2 experiments single or multiple sets of bilateral knife cuts were made in a total of 73 female CFE rats just lateral to the ventromedial hypothalamus (VMH) and/or just medial to the lateral hypothalmus (LH). The lateral VMH knife cuts by themselves produced greater hyperphagia and obesity than did the medial LH cuts. The lateral VMH knife cuts also significantly increased food intake and body weight in Ss previously given bilateral cuts along the medial LH border. Findings indicate that the feeding inhibitory fibers responsible for the hyperphagia syndrome do not project from the VMH to the LH, and this calls for a reevaluation of hypothalamic circuitry. It was also discovered that sham surgery in 7 Ss had a significant suppressive effect on the hyperphagia syndrome produced by hypothalamic knife cuts. (25 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Chonically reduced body weight in rats sustaining lesions of the lateral hypothalamus and maintained on palatable diets and drinking solutions.

12 male Holtzman rats sustaining lateral hypothalamic (LH) lesions regulated their body weight at a reduced level when maintained for 1 mo postlesion upon a wet mash diet. Thereafter, for a period of 84 days, half of these Ss were offered a high fat diet, whereas the remaining Ss continued to receive wet mash. A series of palatable drinking solutions were also offered. Body weight remained at reduced levels relative to 8 intake controls regardless of the diet offered, even under conditions of high fluid intake generated by the palatable drinking solutions. Results contradict the interpretation of E. J. Mufson and R. S. Wampler (see record 1973-00428-001) that the lower body weight observed in LH-lesioned animals is secondary to lesion-produced "finickiness" and/or dehydration resulting from hypodipsia. Rather, a primary shift in the set point for body weight appears to underlie the reduced levels of weight maintenance in LH-lesioned animals. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Attenuation of gastric lesions by psychological aspects of aggression in rats.

In a study with 80 male albino rats, Ss that fought with each other in response to electric shock showed reduced gastric lesions in comparison with Ss that received the same shocks alone so that fighting behavior did not occur. Also, gastric lesions were similarly reduced in Ss that fought even though they could not physically contact one another because of a barrier between them. In this case, the "protective" effect of fighting derived from the release or display of fighting behavior and did not require physical combat. A 2nd experiment with 48 rats showed that Ss that received shock together but did not engage in fighting behavior showed no reduction of gastric lesions, so that the protective effect of fighting was not an artifact of Ss receiving shock together. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Relationship of cervical and abdominal vagal activity to lower esophageal sphincter function

The purpose of this study was to compare the effects of electrical stimulation of the abdominal and cervical portions of the vagus on lower esophageal sphincter (LES) pressure in the anesthetized opossum. Unilateral or bilateral abdominal vagotomy gave no significant change in basal LES pressure or in the sphincteric response to swallowing. Electrical stimulation of the peripheral end of the sectioned cervical vagus gave a frequency-related decrease in LES pressure with a maximum reduction of 93.5 +/- 2.5% at 10 HZ, 10 V. Stimulation of the central end of the cervical vagus increased LES pressure, with a maximum response of 34.0 +/- 1.9 mm Hg. Neither peripheral nor central stimulation of the sectioned abdominal vagus had significant effect on LES pressure (P greater than 0.05). Additionally, LES relaxation in response to swallowing or cervical vagal stimulation was intact after bilateral abdominal vagotomy. These studies suggest that whereas the cervical portion of the vagus mediates inhibitory and excitatory changes in LES pressure, the abdominal vagus has no demonstrable role in the control of LES function.     

Altered food preferences after lesions in the basolateral region of the amygdala in the rat.

Studied the food preferences of 52 male hooded Lister and albino Wistar rats. 19 Ss were intact; 33 received bilateral lesions of the basolateral amygdala. Lesioned Ss chose different foods from controls in 10-min food-preference tests. The normal Ss ate primarily familiar chow, while the amygdala-lesioned Ss ate primarily novel foods. The lesioned Ss did not select indiscriminately but showed definite preferences. With repeated testing, the normal Ss' preferences became similar to those of the lesioned Ss. Food-preference tests in a disturbing environment suggested that the difference between the lesioned and control groups was not due to a general alteration in behavior such as fear. Other aspects of ingestive behavior, such as body weight regulation, were not primarily altered by the lesions. The basolateral amygdala may therefore be concerned with the selection of foods on the basis of previous experience. (24 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The vagus

The surgical physiology of the vagus is reviewed with respect to vagotomy in the treatment of duodenal ulcer. All types of vagotomy (truncal, selective gastric, or proximal gastric) produce similar reduction in acid secretion and comparable elevation in serum gastrin. The evidence is mounting that the vagus may have opposing influences on gastrin release: stimulation and inhibition. Division of only the extragastric vagal branches leads to withdrawal of an inhibitory mechanism rendering the denervated stomach more sensitive to the action of gastrin. The loss of this vagally controlled inhibitory mechanism, rather than more meticulous dissection, may explain the higher incidence of more complete vagotomies in selective than in truncal vagotomy. Proximal gastric vagotomy may be the ideal elective operation yet devised for duodenal ulcer. It does, however, cause elevation in serum gastrin and more than 90 per cent of patients after this operation will have positive insulin test in two to four years. This is higher than the positivity seen with truncal vagotomy. Results of controlled trials are needed before this operation becomes fully established.