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Sleep in the rat during food deprivation and subsequent restitution of food.

Continuous telemetric EEG recordings served to determine the vigilance states of the rat during 2 control days, 80 h of food deprivation and 64 h following restitution of food. The recordings were supplemented by measurements of food intake, water intake and motor activity. The following 3 sleep parameters were not significantly changed by food deprivation: the daily amount of the vigilance states, the light-dark distribution of sleep and waking, and the 10 min paradoxical sleep (PS) cycle. During food deprivation, PS was depressed in the dark phase of the diurnal cycle and increased in the light phase. The sleep parameter that was most affected by food deprivation was the duration of sleep episodes. Episodes of slow-wave sleep (SWS) and PS were shortened only in the dark phase of the deprivation days, whereas total sleep episodes were progressively decreased in both diurnal phases. After restitution of food, the episodes of SWS and total sleep were immediately lengthened and tended to exceed the control level. The duration of feeding episodes and meal size were significantly increased in comparison to pre-deprivation values, whereas feeding frequency was decreased. Long episodes of continuous motor activity occurred during the dark phase of the refeeding period, while a fragmented activity pattern was typical for the deprivation nights. It is proposed that the adjustment of the length of behavioral episodes may constitute an important adaptive mechanism for the rat.

Animals

Food deprivation increases oral and intravenous drug intake in rats.

Rats given continuous access to etonitazene hydrochloride in their drinking water (5 micrograms per milliliter) more than doubled their drug intake while deprived of food. Another group of rats with implanted jugular catheters self-administered etonitazene (10 micrograms per kilogram) intravenously on a continuous reinforcement schedule, and the number of infusions increased significantly on days when they were deprived of food. These results suggest that feeding condition may be a powerful determinant of drug-reinforced behavior.

Administration, Oral

The effects of food deprivation on protein turnover and nucleic acid concentrations of active and immobilized extensor digitorum longus muscles of the rat.

Deprivation of food caused significant changes in the weight, protein content, protein turnover and RNA concentrations of the extensor digitorum longus muscle. Simultaneous immobilization to render the muscle inactive did not make the tissue any more susceptible to the effects of starvation. In contrast, immobilization in a stretched state resulted in less muscle wasting after deprivation of food.

Animals

Effects of food deprivation on etonitazene consumption in rats.

One group of free-feeding rats was given a 5 microgram/ml etonitazene HCl solution as their sole liquid. This group increased their drug intake by 100% when they were partially food-deprived during a 23-day period. Another group that remained food-satiated and received etonitazene for an equal number of days did not show similar increases in drug intake. However, this group drank greater volumes of the etonitazene solution than a food-satiated control group drank of water. These results are contrasted with a fourth group showing a 50% decrement in water intake during similar food-deprived conditions. The food-deprived group drinking etonitazene showed highly erratic drinking patterns compared to all the other groups. Daily liquid intake ranged from 30 to 250 ml in this group, and volumes oscillated from high to low on alternating days. When the food-deprived/food-satiated conditions were replicated in this experimental group, corresponding increases and decreases in drinking reliably occurred. However, during the second food-deprived phase, the large increases occurred almost immediately as contrasted with a gradual increase over 17 days during the first food-deprived phase. This would suggest a learning mechanism may be involved. Self-mutilation and other forms of stereotypy were noted only in food-deprived rats consuming etonitazene.

Animals

Effect of experimental diabetes, food deprivation and genetic obesity on the sensitivity of pithed rats to autonomic agents.

1 The sensitivities of alloxan and streptozotocin diabetic and hereditary obese pithed rats to acetylcholine, isoprenaline and noradrenaline were compared to those of controls. 2 Blood pressure and heart rate recordings made before dosing was started showed the streptozotocin-treated animals to have a significantly reduced heart rate and increased pulse pressure as compared with controls. 3 Both diabetic groups were found to have reduced sensitivities to the pressor effect of noradrenaline, the depressor effect of acetylcholine, the positive chronotropic and inotropic effect of isoprenaline and the reduction in diastolic pressure induced by isoprenaline. The reduction in sensitivity was generally much greater in the streptozotocin diabetic animals. 4 The genetically obese rats were found to have similar sensitivities to all three agents as did their non-obese litter mates. 5 When either diabetic group was deprived of food for 24 h preceding the tests the sensitivities were found to be raised significantly towards normal in almost all cases. 6 The results are contrasted with previous in vitro results and possible causative metabolic factors discussed. It is suggested that sensitivity changes are unevenly distributed within the cardiovascular system.

Acetylcholine

Wheel running of kangaroo rats, Dipodomys merriami, as related to food deprivation and body composition.

Kangaroo rats deprived of food ran themselves to death in 48 h in wheel cages. Despite the loss of 14.5% of body weight the ratio of water to protein was the same after the run as it was in control rats. Metabolic measurements at rest and in the running wheel and weight loss in the 48-h run were used to estimate fuels used and water expended. Two-thirds of the initial amount of fat and 9% of the protein were metabolized. The terminal mean percentage of body fat was about twice that observed in rats trapped in the spring of 1967, when seed production was low: death in the 48-h run could not have been due to depletion of body fat alone. The powerful activity drive seen in hungary kangaroo rats presumably is intensified in dry years when food is scarce and may deplete their reserves enough to result in death from starvation.

Animals

Effects of food deprivation on ketonaemia, ketogenesis and hepatic intermediary metabolism in the non-lactating dairy cow.

1. The aim of this work was to investigate why non-lactating dairy cows are less susceptible to the development of ketonaemia during food deprivation than are dairy cows in early lactation. 2. The first experiment (Expt. A) consisted of determining the effect of 6 days of food deprivation on the concentrations of ketone bodies, and of metabolites related to the regulation of ketogenesis, in jugular blood and liver of non-lactating cows. 3. During the food deprivation, blood ketone-body concentrations rose significantly, but to a value that was only 16% of that achieved in lactating cows deprived of food for 6 days [Baird, Heitzman & Hibbitt (1972) Biochem. J. 128, 1311--1318]. 4. In the liver, food deprivation caused: a rise in ketone-body concentrations; a fall in the concentration of glycogen and of various intermediates of the Embden-Meyerhof pathway and the tricarboxylic acid cycle; an increase in cytoplasmic reduction; a decrease in the [total NAD+]/[total NADH] ratio; a decrease in energy charge. These changes were all qualitatively similar to those previously observed in the livers of the food-deprived lactating cows. 5. There appeared therefore to be a discrepancy in the food-deprived non-lactating cows between the absence of marked ketonaemia and the occurrence of metabolic changes within the liver suggesting increased hepatic ketogenesis. This discrepancy was partially resolved in Expt. B by the observation in two catheterized non-lactating cows that, although there was a 2-fold increase in hepatic ketogenesis during 6 days of food deprivation, ketogenesis from the splanchnic bed as a whole (i.e. gut and liver combined) declined slightly owing to cessation of gut ketogenesis.

Adenine Nucleotides

Effects of various periods of food deprivation on serotonin turnover in the lateral hypothalamus.

Preliminary results indicated enhanced serotonin turnover in the lateral hypothalamus of 24 hr food deprived rats as compared to non-deprived rats. In the present study, the periods of food deprivation were extended in ordered that the effects of 0. 24, 48 and 72 hr of food deprivation on serotonin turnover could be measured. One hr following an infusion of 3H-5-hydroxytryptamine the lateral hypothalamus was perfused with physiological bacteriostatic saline for 40 min. Samples of perfusate, which corresponds to 75--90 min post-infusion, were analyzed by thin layer chromatography for estimation of 3H-labelled precursor and metabolites. The results indicate that serotonin turnover is enhanced as a function of hours of food deprivation.

Animals

Interaction of food deprivation with different measures of amphetamine effects.

The effects of d-amphetamine (0.0, 0.5, 1.0 mg/kg) on feeding, activity, and food-dish contact time of male Holtzman rats were investigated under 4 different levels of food deprivation (0, 12, 24, 36 hr). Differences in the amount of food deprivation significantly influenced the drug's effect on feeding and food-dish contact time, but not on activity. Also, differences in the amount of food deprivation significantly influenced the interrelationship (correlation) of amphetamine's effects on activity and food-dish contact time and on food-dish contact time and feeding, but not so much the interrelationship of the drug's effects on feeding and activity. These findings suggest that the amount of food deprivation differentially influences different general measures fo amphetamine effects as well as differentially affecting the interrelationship of amphetamine effects. The importance of the correlation data to the potential incompatibility of the drug's effects as well as to an interpretation of food-dish contact time is briefly considered.

Animals

The effects of food deprivation and re-feeding on bovine adipose-tissue glycogen synthase.

Bovine adipose-tissue glycogen metabolism was studied during food deprivation and re-feeding. Changes in the specific activity of adipose-tissue glycogen synthase paralleled changes in tissue glycogen content: both parameters increased during food deprivation and remained so during the first 10 days of re-feeding. The values for the A0.5 (activation constant) for glucose 6-phosphate of the freshly isolated enzyme from adipose tissue from fed and starved steers were 2.9 +/- 0.1 mM and 0.90 +/- 0.05 mM respectively. Additionally, whereas incubation of adipose-tissue extracts from fed steers did not activate endogenous glycogen synthase (through a presumed phosphoprotein phosphatase mechanism), the enzyme from starved or re-fed (up to 3 days re-feeding) steers was reversibly activated as measured by changes in the value for the A0.5 for glucose 6-phosphate. Thus activation of bovine adipose-tissue glycogen synthase during food deprivation appears to be related to expression of glycogen synthase phosphatase activity. These effects of food deprivation on bovine glycogen metabolism contrast markedly with the effects observed in rat adipose tissue.

Adipose Tissue

Predation, aggression, and activity levels in food-deprived sunfish (Lepomis macrochirus and L. gibbosus): motivational interactions.

Three experiments investigated the effects of food deprivation on several behavioral categories in two species of sunfish. In Experiment 1, predatory behavior and general activity were observed under five levels of deprivation. For both species, predation measures increased in a similar negatively accelerating manner with increasing deprivation, while activity changed in a more complex fashion. Experiment 2 examined the effects of deprivation on activity in a novel environment and showed that the deprivation effects of Experiment 1 were masked by the response to the new setting. In Experiment 3, measures of aggression toward intruders of each species were recorded from resident fish of both species under three levels of food deprivation. Both species were more aggressive toward conspecifics, and bluegills were more aggressive overall. Aggression was significatly influenced by food deprivation, with the effects dependent on the species making up the pair. Theories of motivational summation, generalized drive, and activity-mediated aggression were unable to explain the differential effects of hunger on the three behavioral categories observed. A dynamic boundary-state model of behavior control was found to predict the motivational interactions observed between distinct behavioral control systems.

Aggression

Turnover of 3H-5-hydroxytryptamine to 3H-5-hydroxyindoleacetic acid and the 3H-5-methoxyindoles in nondeprived and 24 hr food deprived rats.

Serotonin turnover in the lateral in hypothalamus (LH) was determined in nondeprived and 24 hr food deprived rats. The LH was infused with 0.5 muCi of 3H-5-hydroxytrptamine 1 hr prior to push-pull perfusion. The percentage of nCi/muCi of radioactivity was analyzed by thin layer chromatography and liquid scintillation spectrometry. There was significantly more 5-hydroxyindoleacetic acid and 5-methoxytryptamine formed in the 24 hr food deprived rats. These results indicate a faster 5-hydroxytryptamine turnover rate in the LH of 24 hr food deprived rats than in nondeprived rats.

5-Methoxytryptamine

HPLC determination of biogenic amines in discrete brain areas in food deprived rats.

Norepinephrine (NE), dopamine (DA), 5-hydroxytryptophan (5-HTP), 5-hydroxytryptamine (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) levels in the lateral hypothalamus (LH), ventromedial hypothalamus (VMH), median raphe (MR) and dorsal raphe (DR) were determined in nondeprived and 48 hr food deprived rats. Simultaneous determination of these compounds was accomplished by means of high performance liquid chromatography (HPLC) with electrochemical detection. When compared with controls, food deprived animals showed significant increases in 5-HT and 5-HIAA levels in the raphe nuclei, significant increases in 5-HIAA in the LH, but no changes in either 5-HT or 5-HIAA levels in the VMH. No changes in catecholamine levels were found in any of the brain areas studied. These results show that indoles in the raphe nuclei, as well as in the LH, are affected by food deprivation. The lack of change in indole levels in the VMH indicates that specific nuclei within the hypothalamus are differentially affected by food deprivation.

Animals

Catecholamines in some hypothalamic and telencephalic nuclei of food deprived rats.

The influence of 48 h food deprivation on the levels of catecholamines was investigated in different hypothalamic and telencephalic nuclei of the rat brain. There were on changes in the levels of noradrenaline (NA) and dopamine (DA) in the lateral hypothalamic area, dorsomedial nucleus, medial preoptic area and in nucleus of diagonal band (septum). On the other hand we observed a statistically significant decrease of NA and DA in the ventromedial nucleus and the decrease of NA in the arcuate nucleus.

Animals

Effects of marijuana extract distillate and cannabidiol on variable interval performance as a function of food deprivation.

Lever-pressing rates plotted as a function of number of hours of food deprivation produces an inverted U curve, the activation performance curve. Since delta 9-tetrahydrocannabinol depresses the response rate on variable interval (VI) performance, it may be that the response depression reflects changes in this curve. Rats were tested VI performance at five levels of food deprivation and were treated with a vehicle control, marijuana extract distillate (MED) at 7.5 and 11.25 mg/kg, cannabidiol (CBD), at 15 mg/kg or combinations: 7.5 mg/kg MED + 15 mg/kg CBD and 11.25 mg/kg MED + 15 mg/kg CBD. MED produced a depression of VI performance which was greatest at low levels of deprivation. CBD did not depress performance. When CBD was conbined with MED, potentiation of depression occurred. The potentiation depression was not additive, but occurred at high levels of deprivation. It appears that MED depresses performance most at low levels of deprivation and that CBD potentiates the depression produced by MED at high levels of deprivation.

Animals

Pancreatic glucagon, food deprivation and feeding in intact and vagotomized rabbits.

Thirty New-Zealand female rabbits were implanted with hepatic-portal cannulas and six simultaneously underwent bilateral subdiaphragmatic vagotomy. When recovered, all animals received pancreatic glucagon infused at 1.0 cc/min for a total dosage of 12 microgram in 3.0 cc of isotonic saline. On alternate days, isotonic saline alone was infused as a control. Twelve intact and six vagotomized animals received infusions terminating food deprivations of 4, 8, and 24 hr while the remaining animals received the infusions only when free feeding. The feeding behavior of all animals was measured at 0.5, 1 and 2 hr postinfusion. Glucagon significantly suppressed feeding relative to saline only in 0- and 4-hr-food-deprived intact rabbits. Longer deprivations followed by glucagon did not produce suppression, and glucagon was completely ineffective in suppressing feeding in vagotomized animals. Although glucagon infusion in 4-hr food-deprived intact rabbits produced 38% suppression of food intake during the first hr postadministration, glycogen analysis revealed no significant reduction under the behavioral testing paradigm. These results indicate that glucagon can suppress food intake without depletion of liver glycogen. It is suggested that glucagon is not a satiety signal but can probably suppress feeding through initiating glycogenolysis.

Animals

Antipunishment effects of diazepam: interaction with shock and food deprivation levels in pigs.

The effects of 1mg/kg diazepam on punished behaviour of pigs were investigated under various degrees, of food deprivation and/or shock level. Responses emitted during the punishment signal were affected more by the shock level than by the degree of food deprivation while nonpunished response rates were modified by neither factor. Diazepam treatment increased the number of responses emitted during the punishment signal but interacted with the shock intensity: drug effects were attenuated when the shock intensity was severe, in spite of an equivalent control baseline. Diazepam also increased the overall rate of nonpunished responding. The drug treatment had no reliable effect on flinch and escape thresholds measured in separate experiments. The effects of diazepam on punished responding do not appear to be related to eventual changes in food motivation or sensitivity to electric shock.

Animals