Effects of hunger on the responses of neurons in the lateral hypothalamus to the sight and taste of food

Burton, M.J.; Rolls, Edmund T.; Mora, Francisco

doi:10.1016/0014-4886(76)90189-8

Cited by 242 publications

(77 citation statements)

References 7 publications

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“…In relation to this suggestion it is of interest that in the neurophysiological experiments [2,17,18,19] described in the introduction, neurons were found in the hypothalamus of the monkey which ceased to respond to a food with which the monkey had been fed to satiety (yet which still responded to other foods). Additional evidence consistent with the suggestion that the responses of these neurons are involved in whether a food is accepted (or rewarding) is that these neurons were activated by rewarding electrical stimulation of some brain sites, and that brain-stimulation reward in the region of these neurons was attenuated after the monkeys were fed to satiety [20] (see also [16]).…”

Section: Discussionmentioning

confidence: 99%

“…Taste Food intake WHILE recording from lateral hypothalamic neurons which responded to the sight and/or taste of food in the alert behaving monkey, E. Rolls and his colleagues observed that the responses of these neurons became attenuated to the sight and/or taste of the food on which the animal was satiated, but continued to respond to other foods which had not been used to produce satiety [2,17,18,19]. It was also observed that the monkeys continued to accept these other foods while rejecting the food on which they had satiated.…”

Section: Specificity Of Satietymentioning

confidence: 99%

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Sensory specific satiety in man☆

Rolls

Rowe

et al. 1981

Physiology & Behavior

773

421

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. Sensory specific satiety in man. PHYSIOL. BEHAV. 27(1) [137][138][139][140][141][142] 1981.--To investigate the specificity of satiety in man, subjects (n=32) rated the pleasantness of the taste of eight foods, were then given one of the foods to eat for lunch, and re-rated the pleasantness of the taste of the eight foods 2 and 20 rain after the end of the meal. The pleasantness of the food eaten decreased more than that of the foods not eaten (p<0.001). In a second experiment it was shown that this relative specificity of satiety influenced subsequent food intake. Before a first course, subjects (n =24) rated their liking for the taste of eight foods, were then given one of the foods to eat for lunch, and 2 min after finishing eating re-rated their liking for the taste of the eight foods. Again liking decreased more for the food eaten than for foods not eaten. These changes in liking for the foods eaten and not eaten were highly correlated (p <0.001) with the amounts of those foods eaten in an unexpected second course. Thus in man satiety can be partly specific to foods eaten and this specificity may be an important determinant of the foods selected for consumption. Specificity of satietyTaste Food intake WHILE recording from lateral hypothalamic neurons which responded to the sight and/or taste of food in the alert behaving monkey, E. Rolls and his colleagues observed that the responses of these neurons became attenuated to the sight and/or taste of the food on which the animal was satiated, but continued to respond to other foods which had not been used to produce satiety [2,17,18,19]. It was also observed that the monkeys continued to accept these other foods while rejecting the food on which they had satiated. This finding suggests that satiety may not be completely general, but rather may be at least partly specific to the particular food consumed. This led to the present investigation of satiety and its specificity in man. In relation to satiety in man it has been shown that the pleasantness of the taste or smell of food-related test stimuli was decreased by a 50 g load of glucose which was either swallowed or delivered intragastrically [3,4,6,7]. Cabanac and his colleagues I6,8] showed that the glucose load decreased the pleasantness of sucrose solutions but not of salt solutions, and that eating a meal decreased the pleasantness of food-related odors but not of non-food-related odors. They have argued from these findings that there is modulation of the hedonic responses to food produced by the internal nutritional state which could be important in controlling feeding, and have called the phenomenon "alliesthesia" (literally, changing sensation) [3].On the basis of these findings in the monkey and man, we performed the experiments described here, to investigate whether in man there is a satiety mechanism specific for foods eaten. In Experiment 1, the possibility that the pleasantness of the taste of food might decline more for a food eaten than for other foods not eaten was investigated. It was found ...

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Section: Discussionmentioning

confidence: 99%

Section: Specificity Of Satietymentioning

confidence: 99%

Sensory specific satiety in man☆

Rolls

Rowe

et al. 1981

Physiology & Behavior

773

421

View full text Add to dashboard Cite

show abstract

“…It is also of interest that at the stage of the lateral hypothalamus and substantia innominata, at least in the monkey, the responses of the neurons associated with gustatory stimuli occur when the animal is hungry and not when he is satiated (see above and ref. 3).…”

Section: Discussionmentioning

confidence: 99%

“…The effects of satiety on the responses of these neurones associated with the taste of food has been confirmed five times in five different neurones recorded in three squirrel monkeys and two rhesus monkeys (see also ref. 3).…”

Section: (3) the Response Characterandtics Of Neurones In The Lateral Hmentioning

confidence: 99%

Neurophysiological analysis of brain-stimulation reward in the monkey

1980

Self Cite

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SUMMARYNeuronal activity related to brain-stimulation reward and to feeding was analyzed in rhesus monkeys and squirrel monkeys as follows. First, self-stimulation of the lateral hypothalamus, orbitofrontal cortex, amygdala and nucleus accumbens was found. Second, a population of single neurones in the lateral hypothalamus was found to be trans-synaptically activated from one or several self-stimulation sites. It was also found that populations of neurones in the orbitofrontal cortex and amygdala were activated from at least some of the self-stimulation sites. Thus, in the monkey, there is evidence for an interconnected set of self-stimulation sites, stimulation in any one of which may activate neurones in the other regions. These sites include the lateral hypothalamus, amygdala, and orbitofrontal cortex. Third, in one sample of 764 neurones in the lateral hypothalamus and substantia innominata which were activated from brainstimulation reward sites, 13.6 ~ were also activated during feeding, by the sight and/or taste of food. The responses of the neurones with activity associated with taste occurred only while some substances (e.g. sweet substances such as glucose) were in the mouth, depended on the concentration of the substances being tasted, and were independent of mouth movements made by the monkeys. Fourth, the responses of these neurones occurred to food when the monkeys were hungry, but not when they were satiated. Fifth, self-stimulation occurred in the region of these neurones in the lateral hypothalamus and substantia innominata, and was attenuated by satiety. These results suggest that self-stimulation of some brain sites occurs because of activation of neurones in the lateral hypothalamus and substantia innominata activated by the sight

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“…However, an imaging study in a control group of nonobese individuals, 12 together with research from other groups, [13][14][15] has shown that the motivation to eat is controlled by an extensive system of reciprocally connected neural areas, beyond the hypothalamus, mediating both the intrinsically derived hunger drive to eat and the extrinsically derived incentive to eat. 12,16 Key brain regions for the former include the hypothalamus 11,[17][18][19] striatum, 20 orbitofrontal cortex (OFC) [21][22][23] insula [24][25][26] and anterior cingulate cortex, 24 and, for the latter, the amygdala and OFC. [27][28][29][30] Indeed, Lucignani et al 31 have found altered cerebral GABA A receptor function in the insula and cingulate, frontal and temporal neocortices in six adults with PWS compared to controls.…”

Section: Introductionmentioning

confidence: 99%

Neural representations of hunger and satiety in Prader–Willi syndrome

et al. 2005

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Objective: To investigate the neural basis of the abnormal eating behaviour in Prader-Willi syndrome (PWS), using brain imaging. We predicted that the satiety response in those with PWS would be delayed and insensitive to food intake. Design and participants: The design of this study was based on a previous investigation of the neural activation associated with conditions of fasting and food intake in a nonobese, non-PWS group. The findings were used to generate specific hypotheses regarding brain regions of interest for the current study, in which 13 adults with PWS took part (mean7s.d. age ¼ 2976; BMI ¼ 31.575.1; IQ ¼ 7178, six were female). Measurements: Regional cerebral blood flow was measured using positron emission tomography in three sessions: one following an overnight fast and two following disguised energy controlled meals of similar volume and appearance -one of 1674 kJ (400 kcal) and another of 5021 kJ (1200 kcal). Subjective ratings of hunger, fullness and desire to eat, and blood plasma levels of glucose, insulin, leptin, ghrelin and PYY were measured before and after each imaging session. Results: The neural representation of hunger, after an overnight fast, was similar to that found in nonobese individuals in the control study. In contrast, after food intake, the patterns of neural activation previously associated with satiety were not found, even after the higher-energy load. Lateral and medial orbitofrontal cortical activation was associated with consumption of the 400-and 1200-kcal meals, respectively. The medial orbitofrontal activation, however, was only found in those who had shown a large percentage change in fullness ratings following the higher-energy meal. Conclusion: We conclude that there is a dysfunction in the satiety system in those with PWS. These findings suggest that brain regions associated with satiety are insensitive even to high-energy food intake in those with the syndrome. This may be the neural basis of the hyperphagia seen in PWS.

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Effects of hunger on the responses of neurons in the lateral hypothalamus to the sight and taste of food

Cited by 242 publications

References 7 publications

Sensory specific satiety in man☆

Sensory specific satiety in man☆

Neurophysiological analysis of brain-stimulation reward in the monkey

Neural representations of hunger and satiety in Prader–Willi syndrome

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