Interactive effects of deprivation in the albino rat

The interactive effects of feeding and drinking schedules were investigated in three experiments. Twenty-four hour water-deprived rats consumed their entire obligatory water intake prior to feeding, whereas 24-hr food-deprived rats consumed only small quantities of food prior to drinking. This drinking was apparently due to a shift of water stores rather than an actual negative water balance. Experiment 3 investigated the effects of 24, 48, or 72 hr of water, food, or total deprivation. Water-deprived rats did not adequately suppress food intake and became thirstier than totally deprived rats. The effects of total deprivation were essentially identical to those of food deprivation. These experiments indicate the degree to which deprivation schedules impose restrictions on the reinforcement parameters of behavioral experiments.     

The effect of hunger on water intake in rats

Although reciprocal inhibition between eating and drinking has been postulated, the commonly observed reduction of water intake by hungry rats may not be due to any direct inhibitory mechanism. In one experiment rats deprived of food for 24 hr. and then injected with 2 ml. of NaCl drank the same as rats that had received food ad lib. In the second experiment a stomach load of 10 ml. of water 3 hr. before the salt injection was designed to abolish any water deficit that might have occurred during food deprivation had there been inhibition of drinking by hunger. Here again rats deprived of food did not drink less than undeprived animals. In fact the hungry rats drank slightly but significantly more. This phenomenon may be related to the observation confirmed here that during food deprivation rats excrete about twice as much rather dilute urine as during ad lib food intake. This seems to indicate that though in general food deprived rats drink less than normal they actually drink more than they need. Schedule induced polydipsia also occurs during food deprivation and this too makes it unlikely that water-intake is actually inhibited during hunger.     

Concurrent access to two concentrations of orally delivered phencyclidine: effects of feeding conditions.

Two experiments addressed the effects of food satiation and deprivation on oral self-administration of two concurrently available phencyclidine concentrations. In the first experiment, 8 rhesus monkeys self-administered either of two concentrations of phencyclidine ("PCP, angel dust") and water under concurrent fixed-ratio 16 schedules. One concentration was always held constant (0.25 mg/mL) while a series of other phencyclidine concentrations, ranging from 0 (water) to 1.0 mg/mL, was presented in a nonsystematic order. Initially the monkeys were tested while food satiated, and the procedure was then repeated during food deprivation. The monkeys usually selected the higher concentration within the first few minutes of the session, indicating that taste and/or other immediate postingestional effects were important factors. Contrary to a number of previous reports, there were no consistent differences across subjects in the mean number of liquid deliveries or mean drug intake (mg/kg) during food satiation and deprivation. However, for all monkeys the within-session time course of responding during food satiation consistently differed from that during deprivation. A second experiment assessed whether the failure to find consistent differences in drug intake during food satiation and deprivation had been due to the history of concurrent access to different phencyclidine concentrations or to the extended experience with phencyclidine under food-satiation conditions. Six additional monkeys (Group 2) were exposed to the phencyclidine self-administration procedure (during food satiation and deprivation) for the same length of time as the monkeys in Experiment 1 (Group 1), except they received only concurrent access to phencyclidine (0.25 mg/mL) and water. Both groups then received concurrent access to phencyclidine and water during five repeated cycles of food deprivation and satiation. There were also marked individual differences in Group 2: During food satiation, 2 of the monkeys' responding increased, 1 showed no change, and 3 decreased. Examination of a number of historical variables indicated that the greater the percentage of total sessions spent during food satiation with phencyclidine available (before these experiments began), the greater the amounts of phencyclidine consumed during food satiation and the smaller the differences in phencyclidine intake when the two feeding conditions were compared.     

The octopus in the laboratory. Handling,maintenance, training

Octopus maya lives well for long periods in a small tank containing a plastic house in which it can be carried without disturbance to and from an experimental situation. Data are reported on the growth of animals kept under these conditions as a function of feeding schedule and on their food intake as a function of deprivation. Some animals were trained in a runway with food as reward, and others were trained in a simple maze with return to sea water as reward.     

Four effects of exogenous insulin on food intake

After a subcutaneous injection of bovine insulin into the rat, at first there is an augmentation of the satiety produced by nutrient eaten immediately before injection. Later, with large enough doses, as has been commonly observed, feeding is elicited—perhaps simply by hastening the passage of satiety. A third type of effect is behavioural disruption, reducing food and water intake when food is withheld for an hour after injection and producing postural changes even when food is present. Fourth, repeated pairing of insulin injection with intake of water of a particular flavour (even when drunk over half an hour beforehand) depresses subsequent intake of water having that flavour, whether presented alone or together with water of another flavour which has been paired with control injections. The acquired discriminated intake change involves the initial acceptability of the flavour but changes in the inhibition of acceptability during an intake bout have not been excluded.     

Effects of gastric loads and food deprivation on subsequent food intake in suckling rats.

Suckling rats were subjected to deprivation periods of 6-8 hr. Intake following deprivation was greater in deprived than in nondeprived sucklings, but did not increase with increasing deprivation. Gastric loads of NaCl solutions depressed subsequent intake; 3% NaCl was more effective than .9% NaCl. Other gastric loads of varying osmotic and caloric value also depressed subsequent intake. In order of increasing effectiveness in depressing intake, the gastric loads were protein hydrolystate, heavy cream, water, milk, lactose, glucose, and corn oil. Effectiveness was unrelated to osmotic or caloric value of the load. Gastric fill and, possibly, some property of carbohydrate appear to be important determinants of satiety in the suckling rat.     

Separate neural sites for d-amphetamine suppression of mouse killing and feeding behavior in rats

The present study was conducted to investigate several possible neural sites for d-amphetamine's effect on mouse killing and feeding behaviors. d-Amphetamine (10, 20, and 30 μg) injected into each lateral ventricle, suppressed mouse kiling, food, and water intake in a dose-dependent manner. Bilateral adminstration of d-amphetamine (20 μg) into the central amygdaloid nucleus abolished mouse killing behavior but did not affect feeding and drinking. By contrast, bilateral amphetamine injections into the substantia nigra, or into the ventral region of the caudate nucleus, did not suppress mouse killing behavior, but significantly decreased food and water intake. The lateral hypothalamus was sensitive to d-amphetamine injections, which suppressed mouse killing and food intake as well as water intake. d-Amphetamine injections into the nucleus accumbens produced inconsistent effects on mouse killing and feeding. Our observations suggest a differentiation of the neural sites that mediate feeding from those underlying mouse killing behavior.     

Abdominal vagotomy disrupts food-related drinking in the rat

Rats 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 rats drank after significantly longer latencies and drank significantly less water in 1 hr than did sham-vagotomized (Sham) rats after eating the same size meal (solid or liquid) as Shams. Rats with incomplete vagal transection (Vgx-I) ate and drank like Shams. Water intake of Sham and Vgx-I rats correlated positively with the meal size of solid food, but the water intake of Vgx-C rats did not. The failure of Vgx-C rats 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 rats emptied equivalent volumes of liquid food from the stomach into the intestine within 10 min of food entering the stomach. These results indicate that the abdominal vagus is an important neurological substrate for food-related drinking in the rat.     

Antidipsogenic role of the E-prostaglandins

Prostaglandin E1 (PGE1) is antidipsogenic when administered into the lateral cerebral ventricle of the rat. In these experiments PGE1, at a dose of 1 microgram, suppressed water intake induced by centrally administered angiotensin II (AII) or carbachol, subcutaneously administered polyethylene glycol, and water deprivation. Even at this high dose, PGE1 did not reduce water intake due to cellular dehydration. As the dose of PGE1 was reduced, its suppressant effects became more specific to AII-induced drinking, with a dose of 10 ng yielding a significant suppression only in the case of AII-induced drinking. Even at a high dose (1 microgram), the PGE1 suppression of ingestion was specific to water intake. Although PGE1-treated rats reduced food intake if they were not hydrated prior to access to food, no reduction in food intake was seen when they received water by gavage before food presentation. Since PGE-like substances are synthesized in the brain, these data suggest the possibility that the prostaglandin may be involved in the regulation of water balance as a component of a reciprocal system in which water intake initiated by the activation of the renin-angiotensin system is halted by the synthesis and release of PGE.     

Food and water intake as functions of resource consumption costs in a closed economy.

In two experiments, rats living in a closed economy were offered continuous, concurrent access to four resources: food, water, a nest, and a running wheel. Costs of consuming food and water were imposed with bar-press requirements, and the price of either one or both resources was raised. As the consumption cost increased, less was consumed in each bout of resource use. Bout frequency increased, but not sufficiently to compensate for the fall in bout size, and total intake fell. Food and water tended to be complementary resources, in that as intake of one fell with its price, intake of the other also decreased. This interaction was accounted for by the defense of the ratio of body water to lean body mass. As amount consumed decreased, increases in feed efficiency (weight gain per unit of food ingested) and the use of stored calories compensated for the reduced energy intake. There was evidence of competition between feeding and drinking at the higher costs: When both commodities were expensive, the decline in the intake of each one was greater than when only one commodity was expensive. Although the time spent nesting, running, and in unmonitored activity was adjusted when feeding or drinking took more of the rat's day, there was no particular activity that was sacrificed.     

Peripheral control of drinking: gastrointestinal filling as a negative feedback signal, a theoretical and experimental analysis.

The studies described here investigated the hypothesis that the osmotic postingestional satiety signal proposed by McCleary operates through a mechanism related to gut filling rather than by osmotically induced shifts of fluid from osmoreceptors in the brain. A control theory model is presented, which was designed to make quantitatively explicit the hypothesis under question. The results showed that when mannitol, which is not absorbed from the intestine, is added to a highly palatable saccharin-glucose mixture, the amount of fluid consumed decreased in inverse proportion to the mannitol concentration. Mannitol was also shown to block fluid absorption from the intestine at a low concentration (approximately .070 M) and at higher concentrations to lead to a net flux of fluid into the intestinal lumen. It was also shown that mannitol in concentrations that reduced the intake of the palatable solution did not induce thirst when the animals were in water balance. It did induce thirst, however, when the animals were tested in a state of negative water balance. The results of these studies, considered as a whole, support the view that McCleary's osmotic postingestional satiety signal acts as an intestinal distention signal rather than by inducing thirst. The model is found to be reasonably accurate as a first approximation, and suggestions are made for improvements.     

Rats (Rattus norvegicus) modulate eating speed and vigilance to optimize food consumption: effects of cover, circadian rhythm, food deprivation, and individual differences.

The eating behavior of rats (Rattus norvegicus) given food pellets of specified size was examined as a function of environmental, circadian, and experiential influences. Eating times were shorter in lighted, exposed environments than in dark, covered environments, even though in novel, exposed conditions the rats made many scanning movements as they ate. Eating time also varied as a function of the circadian cycle in that eating times were shorter in the night portion of the day-night cycle. Finally, eating times decreased if rats were food deprived, and deprivation had a small but enduring influence. Within the tests there were differences in the eating times of individual rats that were not attributable to the experimental manipulations. That rats can optimize food intake by varying eating speed is discussed in relation to physiological regulation of feeding and to optimal foraging theory.     

Interactions between the effects of food and water motivating operations on food‐ and water‐reinforced responding in mice

Two experiments examined interactions between the effects of food and water motivating operations (MOs) on the food‐ and water‐reinforced operant behavior of mice. In Experiment 1, mice responded for sucrose pellets and then water reinforcement under four different MOs: food deprivation, water deprivation, concurrent food and water deprivation, and no deprivation. The most responding for pellets occurred under food deprivation and the most responding for water occurred under water deprivation. Concurrent food and water deprivation decreased responding for both reinforcers. Nevertheless, water deprivation alone increased pellet‐reinforced responding and food deprivation alone likewise increased water‐reinforced responding relative to no deprivation. Experiment 2 demonstrated that presession food during concurrent food and water deprivation increased in‐session responding for water relative to sessions where no presession food was provided. Conversely, presession water during concurrent food and water deprivation did not increase in‐session responding for pellets. These results suggest that a) the reinforcing value of a single stimulus can be affected by multiple MOs, b) a single MO can affect the reinforcing value of multiple stimuli, and c) reinforcing events can also function as MOs. We consider implications for theory and practice and suggest strategies for further basic research on MOs.     

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.     

Increased eating in rats deprived of running

Daily food intake in rats was temporarily reduced by the introduction of an activity wheel and temporarily increased by the subsequent removal of the wheel. When this outcome is coupled with the positive relation between food deprivation and running—and food deprivation is seen as a loss of eating rather than as a physiological state—there is the suggestion that the total behavior output of the organism may be regulated as such. Specifically, when the rat is deprived of a behavior that recurrently comprises a large part of its total daily activity, an increase may occur in some other behavior.     

Control of instrumental behavior by deprivation stimuli

In Experiment 1, rats were given one trial per day in a straight alley under food deprivation on half of the trials and under water deprivation on the other half. Wet mash was available in the goal box under food deprivation for Group H and under water deprivation for Group T, the other deprivation being nonrewarded for each group. After 15--18 trials both groups ran significantly faster on their rewarded than on their nonrewarded deprivation days. A third group showed that random variation of alley color retarded formation of the discrimination. A fourth group was run in a conditional discrimination in which under food deprivation wet mash was available in a black alley, nonreward in a white alley, and vice versa under water deprivation. This group took 114 trials to begin running significantly faster in their rewarded than in their nonrewarded alley under each deprivation. In Experiment 2, it was shown that prior learning about deprivation cues "blocks" learning about alley color when alley color is subsequently presented in compound with the deprivation cue but that when both alley color and deprivation cues are relevant from the start of training, the rat learns about both cues. It is suggested that previous studies have underestimated the importance of deprivation cues by using conditional discrimination designs, choice measures rather than speeds, and parameters that are not optimal for discrimination learning.     

Nothing gained: An explorative study of the long‐term effects of perceived maternal feeding practices on women's and men's adult BMI,body image dissatisfaction,and disordered eating

The objective of the studies presented here was the prediction of adult body mass index (BMI), body image dissatisfaction, and disordered eating from recalled maternal child feeding practices. Studies 1 and 2 sampled women from the community, and found that recalled childhood feeding practices predicted both current BMI and current disordered eating. Daughters whose mothers pressured them to eat as children had lower BMIs as adults. The more a mother was concerned about her daughter's weight as a child, and the more she restricted fatty food intake, the less the woman was satisfied with her current body image. Disordered eating of adult women was positively related to their mothers' restriction of their fatty food intake as children, and negatively related to the mothers' monitoring of their food intake as children. Combining the samples and subdividing them into four BMI intervals showed that the obese women were higher on all but one of the recalled maternal child feeding practices, as well as on disordered eating and body dissatisfaction. Age was found to be positively related to BMI and drive for thinness, but not to body dissatisfaction or disordered eating, with older women having higher BMI and more drive for thinness. Study 3 sampled adult men from the community and found that recalled maternal child feeding practices predicted adult BMI and disordered eating for men, as well as for women. Considerable sex differences were found for all study variables. Recollection of maternal child feeding practices may have a formative role in the development of body image, disordered eating, and BMI for men and women, even into adulthood.     

Medial septal lesions: disruptions of microregulatory patterns and circadian rhythmicity in rats

The microregulatory patterns of food and water intake were examined in male and female rats bearing medical septal lesions and in sham-operated controls. Medial septal ablation, although not affecting the total amount of food or water ingested, resulted in a profound disruption of the pattern of intake. Circadian rhythmicity was disrupted for a period, returning to normal by 25 days postlesion. Permanent disruptions occurred in feeding patterns in the rats with septal lesions ingested more frequent but smaller meals. There was also a marked increase in food-intake-associated drinking and a decrease in non-food-intake-associated drinking. The results are interpreted to reflect two separate independent effects, a general circadian disruption and an alteration in requlatory behavior produced by a chronic depletion of body fluid.     

Inhibition and working memory: effect of acute sleep deprivation on a random letter generation task]

The literature contains inconsistent data on the effects of acute sleep deprivation on the superior cognitive functions. The primary purpose of this study is to determine the effectiveness of inhibition, one of the functions of the working memory executive centre (EC), over an extended, 36-hour waking period. Inhibition is a cognitive mechanism whereby individuals ignore non-relevant information recorded in their working memory. We also tested the effects of a 36-hour period of acute sleep deprivation on simple reaction time. Twelve young, healthy volunteers (M = 21.5 years, sigma = 2.3) performed a random generation task involving letters and a simple reaction time psychomotor test over four sessions held at 10-hour intervals. Each participant was assigned a "constant routine." Participants were kept awake in a prone position within a room whose environment was held strictly constant (light, noise, temperature, meals, etc.). This control procedure provided assurance that any variation in participant performance was solely caused by sleep deprivation. The random generation task, nearly two minutes in length, consisted in verbally producing a sequence of 100 letters in a random fashion (i.e. by inhibiting, for example, alphabetical order) and by keeping to a set rhythm. Our assumption was that capacity for inhibition diminished as the number of hours of sleep deprivation increased. The simple reaction test, 10 minutes in length, involved pressing a button as swiftly as possible to cause a black square to disappear from a screen. In this case our assumption was that acute sleep deprivation alters simple reaction time. Analysis of variance (ANOVA) through repeated measures using the "sessions" factor as an intra-subject variable showed no significant changes in randomization indices of the random generation task, contrary to analysis of average simple reaction times. Participants' reaction times deteriorated over the first two minutes of the test during the night they were deprived of sleep. It would seem that the contradictory results of previous studies of the effects of acute sleep deprivation on the inhibition function would be due to errors in factor identification. In conclusion, the inhibition function, as measured during the performance of a brief task, seems to remain intact during an extended, 36-hour waking period. Simple reaction time assessed by means of a brief psychomotor test is affected during a night of sleep deprivation. The working-memory inhibition executive function shows greater resistance to acute sleep deprivation than does psychomotor reaction time for the performance of short tasks.     

Cholecystokinin elicits the complete behavioral sequence of satiety in rats.

The behavior of intact rats and rats with chronic gastric fistulas was observed and scored during a 60-min test period when they were offered liquid diet after 17 hr of food deprivation. Intact rats and rats with closed fistulas displayed a specific behavioral sequence at the end of each meal: They stopped eating, engaged in grooming and exploration for a short time, and then rested or slept. Thus, a fixed behavioral sequence characterizes satiety in the rat. Although the behavioral sequence of satiety was fixed, the cessation of feeding was not a sufficient condition for the appearance of the rest of the sequence: Quinine adulteration of the liquid diet stopped sham feeding but did not elicit the complete sequence. Intraperitoneal injection of the intestinal hormone cholecystokinin during sham feeding, however, elicited the complete sequence of satiety. The observation that cholecystokinin not only stops feeding but elicits the complete sequence of satiety supports our hypothesis that endogenous cholecystokinin is a satiety signal for the rat.