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E T Rolls

Publications and source records attributed to E T Rolls.

At least 163 records · Page 9Linked to original sources

Satiety role of the small intestine examined in sham-feeding rhesus monkeys.

A sham-feeding preparation utilizing rhesus monkeys was employed to investigate the anatomical site of origin of satiety signals in the gastrointestinal tract. A series of experiments in which food was diverted from the stomach, the small intestine, or both demonstrated that (a) food acting at the pregastric level is not sufficient to produce normal-sized meals, (b) the accumulation of food in the small intestine is necessary to produce normal-sized meals, and (c) a potent preabsorptive or postabsorptive satiety signal originates at the intestinal level. This unidentified satiety signal is sufficient to elicit satiety, can be dissociated from gastric emptying, and does not require the presence of gastric distention to operate.

Animals↗

Neurophysiological analysis of brain-stimulation reward in the monkey.

Neuronal 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 to 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 brain-stimulation 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 and/or taste of food in the hungry animal, and that these neurones are involved in responses to food reward.

Amygdala↗

Drinking in the rhesus monkey: peripheral factors.

Rhesus monkeys prepared with chronic cannulae implanted in the stomach and duodenum were water deprived for 22.5 hr. With both cannulae closed, a mean of 137 ml was drunk within a 60-min period. When ingested water drained freely from an open gastric cannula, continuous drinking far in excess (878 ml mean intake) of normal occurred. Sham drinking also exceeded (634 ml mean intake) normal when ingested water drained through an open duodenal cannula. This pattern of continuous sham drinking indicates that oropharyngeal stimulation is not sufficient alone, or together with the passage of water through the stomach and the initial part of the duodenum, to terminate drinking. Duodenal infusions of water (25-100 ml) slowed or stopped gastric sham drinking in a dose-dependent fashion, but equivalent infusions of isotonic saline were without effect. Thus, pre- or postabsorptive signals at or beyond the level of the intestine distal to the site of the duodenal cannula are probably important for the termination of drinking in the rhesus monkey.

Animals↗

Drinking in rhesus monkeys: role of presystemic and systemic factors in control of drinking.

The effect of 24-hr water deprivation and subsequent drinking on systemic fluid balance was determined in rhesus monkeys prepared with indwelling cardiac catheters. Significant intracellular and extracellular depletions, as indicated by increased plasma sodium concentrations, osmolality, and plasma protein concentrations, resulted from the deprivation. An early attenuation in rehydrational drinking rate (2--4 min) was not associated with changes in systemic fluid balance, which suggests presystemic influences on behavior at this time. When drinking terminated (10 min), however, plasma dilution was significant. In experiments in which monkeys were sham drinking (open gastric cannula), water but not isotonic saline infusions, given through an intestinal cannula, reduced drinking rate and produced significant plasma dilution. Intravenous water infusions reduced drinking to only a comparable extent despite more rapid and substantial plasma dilution. Thus, systemic absorption does not account entirely for the effect of intestinal water infusions on drinking. It is concluded that stimulation of mechanisms both presystemically (within the intestine or the hepatic portal circulation) and systemically is important in the control and termination of rehydrational drinking in this species.

Animals↗

Thirst following water deprivation in humans.

The effect of 24-h water deprivation and subsequent drinking on systemic fluid balance and subjective sensations has been determined in human beings. The deprivation caused significant intracellular and extracellular depletions, thirst, and a dry unpleasant tasting mouth. During rehydration, subjects drank 65% of their total intake within 2.5 min. The marked decrease in drinking rate thereafter, and the alleviation of thirst, occurred before plasma dilution had become significant. This attenuation of drinking was subjectively attributed to stomach fullness. Presystemic factors may therefore be important for drinking termination in humans. Within 20 min systemic deficits were removed, but intermittent drinking continued at a low rate, reportedly to alleviate unpleasant oral sensations, Following rehydration, the concentrated urine of hydropenia had disappeared. However, the excretion of solute-free water varied between subjects. Plasma renin activity was significantly elevated by water deprivation, while after rehydration this activity had decreased to levels not significantly different from predeprivation values.

Adult↗

Bombesin suppresses feeding in rats.

Bombesin (BBS) is a tetradecapeptide originally isolated from amphibian skin1. BBS-like immunoactivity is widely distributed in mammalian gut2-5, and plasma levels have been shown to rise sharply following feeding (ref. 6 and V. Erspamer, personal communication). The physiological actions of BBS are unknown. We have previously shown that the classic gut hormone cholecystokinin (CCK) is a powerful and specific suppressor of food intake7-9. Although CCK and BBS lack common amino acid sequences, they have certain common actions on gut viscera10,11. We have now shown that BBS also suppresses food intake, and we compare its action with that of CCK.

Animals↗

Intracranial self-stimulation in orbitofrontal cortex and caudate nucleus of rhesus monkey: effects of apomorphine, pimozide, and spiroperidol.

Rhesus monkeys were prepared with stimulating electrodes implanted into the orbitofrontal cortex and head of the caudate nucleus under stereotaxic control. These regions of the brain contain high levels of dopamine, and intracranial self-stimulation was readily elicited from these loci in all animals tested using licking behavior as the operant response. Self-stimulation at both sites was significantly attenuated following peripheral injections of the dopamine receptor blocker spiroperidol (0.02 mg/kg). Similarly, pimozide (0.15 and 0.20 mg/kg) significantly reduced self-stimulation in the orbitofrontal cortex, but the suppression observed at caudate placements did not reach statistical significance. Licking for a reward of blackcurrant juice was unaffected by either drug. Apomorphine (0.2, 0.4 mg/kg) had a differential effect on self-stimulation. This drug significantly attenuated self-stimulation in the orbitofrontal cortex, while the same treatment tended to facilitate self-stimulation in the caudate. Apomorphine did not significantly affect responding for the fruit juice reward. The parallels between the effects of dopamine agonists and antagonists on self-stimulation in the monkey and rat suggest that dopamine influences self-stimulation of some sites in both the primate and the rat.

Animals↗

The latency of activation of neurones in the lateral hypothalamus and substantia innominata during feeding in the monkey.

To investigate whether the responses of neurones in the lateral hypothalamus and substantia innominata associated with the sight of food could control the responses of the hungry monkey to the food, the latency of activation of these neurones by food was measured. It was found that when an electromagnetically operated wide-aperture shutter opened to reveal food or non-food objects, these hypothalamic neurones responded with a latency of 150--200 msec to the food objects, and did not respond to the non-food objects. To measure the latency of the monkey's responses to the food, a visual discrimination task was set in which the monkey could lick a tube to obtain fruit juice if a food-realted visual stimulus was shown, but obtained hypertonic saline, which was aversive, if a different visual stimulus was shown. In this situation the typical latencies of the neuronal responses to the food were 150--200 msec, of the lick responses 350--500 msec, and of the EMG activity associated with these lick responses 250--400 msec. Thus the responses of these hypothalamic neurones precede the monkey's responses to the food, and could mediate the feeding and other responses of the animal to the food. It was also shown that a different population of hypothalamic neurones with responses associated with the sight of aversive visual stimuli had response latencies of 150--200 msec.

Animals↗

Effects of satiety on self-stimulation of the orbitofrontal cortex in the rhesus monkey.

Self-stimulation of the orbitofrontal cortex of the rhesus monkey was found to be attenuated after the monkeys were fed to satiety. Self-stimulation at some other sites (e.g. the nucleus accumbens septi, the region of the substantia nigra, and the caudate nucleus) was relatively unaffected in the same test sessions by the satiety. In recordings from single neurons in the monkey orbitofrontal cortex, neurons of the type found in the lateral hypothalamus with sustained responses associated with the sight of preferred foods were not found. However, some orbitofrontal neurons did respond to the removal of food or other desired objects. These experiments show that self-stimulation of the monkey orbitofrontal cortex in modulated by hunger, and show that some orbitofrontal neurons have complex responses which could be related to the control of feeding.

Animals↗