Schedule and quinine induced deprivation in feeding and refeeding

Twenty female albino rats were adapted to either 0 or 23 hr of food deprivation. Half of each group was then fed 0.125% quinine sulfate adulterated diet for seven days. Following the quinine feeding, ad lib feeding (refeeding) was instituted for 14 days. Several conclusions were drawn from the results: (1) rats on a deprivation schedule fail to show a predicted change to regulation on the basis of taste rather than calories; (2) rats on food deprivation actually increase their relative intake of water; (3) refeeding after a deprivation schedule does not lead to depression of initial intake below normal, but otherwise the process of recovery follows the same course as after total starvation.     

Dietary control of food intake in cats

Control of food intake was studied in adult cats with calorically diluted diets. Any changes in the physical properties of the diet led to a transient reduction in daily food intake that gradually recovered to the baseline level of intake. The cats did not increase their level of food intake on the diluted diets and lost weight. These results are discussed in relation to the feeding ecology of cats.     

Reduced salivation in rats following ventromedial hypothalamic lesions

Salivation was assessed in normal rats and rats with bilateral lesions of the ventromedial hypothalamus (VMH). VMH lesioned rats demonstrated a reliable reduction of salivation. This hyposalivation occurred during a one month period that animals were maintained on dry rat chow and for a 16 day period that animals were maintained on a palatable liquid diet. VMH rats did not differ from control rats in the amount of saliva secreted in response to Prostigmin or wintergreen solution. Thus, while the VMH rat shows a reduced basal salivation level, such animals salivate normally in response to a strong taste substance.     

A re-examination of the ventromedial hypothalamic paradox

Early studies of hypothalamic function found that damage to the ventromedial hypothalamus (VMH) resulted in marked overeating but inferior performance in food-motivated tasks, leading several investigators to conclude that hyperphagic VMH animals were actually less hungry than normal animals. However, numerous studies have since demonstrated that under certain conditions VMH-damaged animals will work as hard or harder for food, and consume as much or more of an unpalatable diet, than normal animals. A review of these experiments suggests that most of the deficits in food-motivated behavior are the result of two dysfunctions, one obesity induced, and the other a direct result of the lesion that can be greatly alleviated by preoperative adaptation. Explanations of the VMH paradox are also examined, and it is concluded that most are too narrow in scope, generally ignoring the fact that obesity and preoperative adaptation have similar effects on thirst- and some avoidance-motivated behaviors. It is proposed that the impaired performance of VMH-lesioned animals in food-reinforced tasks is largely the result of obesity- and lesion-induced dysfunctions that are not specific to either hunger- or thirst-motivated behaviors.     

Feeding response to regulatory challenges after 6-hydroxydopamine injection into the brain noradrenergic pathways

Previous studies have demonstrated that intra-mesencephalic 6-hydroxydopamine (6-OH-DA) injection into the ascending noradrenergic bundles produces hyperphagia in rats. In the present study, 6-OH-DA-injected, hyperphagic rats responded like normals to manipulation of certain factors concerned with the short-term regulation of feeding. First, norepinephrine-depleted animals and controls ate similar amounts after insulin challenge. Second, adulterating the diet with quinine, saccharin or a very palatable cheese resulted in only small and nonsignificant differences in intake in the 6-OH-DA rats and controls. However, a third experiment demonstrated that the long-term regulation of calorie balance was functioning suboptimally in the 6-OH-DA-injected rats. These animals took twice as long as controls to reduce their intake to isocaloric levels after being given a calorically concentrated diet. Thus, a disruption in the efficient calorie regulating mechanism may be a factor leading to overeating after norepinephrine loss. In addition, this study further supports the notion that hyperphagia and finickiness are dissociable.     

The dopaminergic mediation of a sweet reward in normal and VMH hyperphagic rats

The role of dopamine in mediating the rewarding quality of a sweet saccharin-glucose (SG) solution was investigated by comparing the effects of the dopamine receptor blocker pimozide, the bitter adulterant quinine, and solution dilution on the consummatory response to the solution in normal and VMH rats. Experiments 1 and 2 demonstrated that pimozide and quinine caused a dose/concentration dependent reduction in the intake of and the licking response to a SG solution. Pimozide treatment caused an equivalent suppression in the intake of the normal and VMH rats, in both the dynamic and static phases, whereas quinine adulteration caused a greater suppression in the intake of the VMH rats. The effects of pimozide and quinine on initial lick rate were also different. Experiment 3 demonstrated that dilution of a SG solution produced a concentration related decrease in intake and licking response. Dilution of the SG solution, like pimozide treatment, affected the intake of the normal and VMH rats in an equivalent manner. The effects of solution dilution and pimozide treatment on the licking response were also similar. The results suggest that the mechanisms by which pimozide and quinine reduce the hedonic quality of natural rewards are functionally dissimilar. The similarity between pimozide treatment and solution dilution suggests that pimozide reduces the positive affective quality of natural reinforcers. The results are discussed in terms of the dopamine theory of reward, the role of dopamine in hypothalamic hyperphagia, and VMH finickiness.     

Behavioral changes following VMH lesions in rats with controlled insulin levels

The effects of ventromedial hypothalamic (VMH) lesions were studied in female rats made diabetic with streptozotocin that were given twice daily injections of protamine zinc insulin (0.75 μ/100g/day) and in non-diabetic animals of the same sex. Hyperphagia resulted from VMH lesions in both diabetic animals whose insulin levels were controlled and in non-diabetic animals. All animals with lesions exhibited persistent increases in feeding during the light protion of the light—dark cycle. Significant increases in body weight gain were observed in both diabetic and non-diabetic lesioned animals, but the magnitude of weight gain was greater after VMH lesions in non-diabetic rats. VMH lesions also reduced wood-gnawing and increased emotinality, aversion to quinine and reactivity to electric shock. None of the behavioral changes were dependent on hyperinsulinemia, although hyperinsulinemia may contribute to the magnitude of certain of these effects.     

Ventromedial hypothalamic syndrome: Finickiness?

Female rats with lesions of the ventromedial hypothalamus (VMH) underate and lost weight compared to same-diet control rats when fed a 0.2% quinine-adulterated wet-mash maintenance diet, yet overate and gained weight compared to same-diet control rats when fed a 0.4% quinine-adulterated high-fat maintenance diet. Control rats underate and lost comparable amounts of body weight when fed either adulterated diet. These data question the generality of the concept of VMH finickiness and are discussed in terms of an increased hunger hypothesis.     

Effects of quinine adulterated diets on the food intake and body weight of obese and non-obese hypothalamic hyperphagic rats

Female rats given knife cuts between the medial and lateral hypothalamus overate and became obese on a high fat diet. When switched to a quinine diet the knife cut rats initially underate and lost weight, but their body weights did not fall significantly below that of controls maintained on the same diet. Knife cut rats also maintained weights at control levels when given a moderately bitter quinine diet immediately after surgery, but displayed subnormal weights when switched to a very bitter diet. Cuts lateral to the fornix produced a greater weight suppression on the quinine diet, but a smaller weight gain on a high fat diet than did cuts medial to the fornix. The results indicate that the hypothalamic knife cuts elevate the upper limit of body weight with little or no change in the lower body weight limit, and that obesity rather than hypothalamic damage per se is the major cause of the hyperphagic rat's finickiness to unpalatable quinine diets. A dual lipostatic model of the hypothalamic hyperphagia syndrome is discussed.     

The taste of sickness: lipopolysaccharide-induced finickiness in rats

Decrease in food intake is one of the most documented non-specific symptoms of inflammatory processes. However, attention has been mainly focused on quantitative analysis. The present paper reports studies undertaken to test the possible contribution of changes in taste processes in inflammatory-induced alteration of feeding behavior. In a first experiment, the effects of lipopolysaccharide-induced sickness were assessed on preference for saccharin and aversion for quinine in rats using the two-bottle test paradigm. In a second experiment, effect of lipopolysaccharide (LPS) on the behavioral reactivity to palatable, unpalatable and mixed solutions was analyzed using the taste-reactivity paradigm. Our results show that LPS decreased total fluid intake but did not change taste responses to unpalatable or palatable substances. However, LPS increased aversive reactions and decreased hedonic responses to mixed taste. These LPS-induced changes are interpreted as an increase in finickiness and are discussed in regard to their potential role in the adaptation of individuals to sickness.