Continuing Commentary elicits atropine-resistant hippocampal rhythmical slow activity and neocortical low voltage fast activity (LVFA)

of the original article: This article examines how the depletion and replenishment of various energy stores give rise to periodic eating and how constant body-energy levels are maintained over time. Measures of the energy expended throughout the 24-hour feeding pattern in rats indicate that two different energy stores (one of small capacity and one of large) determine two superimposed feeding periodicities: one from meal to meal (prandial), the other from day to night (nyethenieral). The article reviews how experimental overrepletion or overdepletion of gastrointestinal content, blood glucose, or body fats affects food intake. These data suggest that gastrointestinal content determines both meal size and mealTHE BEHAVIORAL AND BRAIN SCIENCES (1983) 4 743 Continuing Commentary to-meal periodicity. Other evidence indicates that glucose uptake rate in tissues, which is modulated by fat synthesis and fat mobilization, affects the periodic onset of feeding and the difference between nocturnal and diurnal postprandial satiety. There follows an examination of the neuroendocrine bases for the interacting mechanisms governing energy input and output balance and of the role of the ventromedial hypothalamus in body-fat regulation and the lateral hypothalamus in feeding. The chronobiological pattern of opiaterelated hyperphagia is different from the dual periodicity of monotonous food intake M. Apfelbaum and A. Mandenoff Laboratory of Human Nutrition, Department of Physiology, Faculty Xavier Bichat, 75018 Paris, France Common sense suggests that a hungry subject derives a certain pleasure from eating, and that satiation is contemporaneous with the disappearance of this pleasure. Thus the hunger-satiety loop implies changes in pleasure. Any experimental model that is particularly relevant to the frequent disturbances of food intake observed in our society is that of "cafeteria"induced hyperphagia in the rat, already mentioned by Le Magnen (1981). As shown by Sclafani and Springer (1976), Rolls, Rowe, and Turner (1980) and Rothwell and Stock (1979) a highly palatable diet (ordinary chow supplemented with four highly palatable items changed every day) provokes hyperphagia and overweight. After 17 weeks of feeding our animals such a diet, we injected them with naltrexone, an opiate antagonist, and a food-intake test was performed during the three following hours (a span of time consistent with the availability of naltrexone); naltrexone reduces "cafeteria"-induced hyperphagia (Apfelbaum & Mandenoff 1981b). When the injection is given at the onset of the light period (Apfelbaum & Mandenoff 1981a), it does not significantly modify the chow intake of the control animals; however it reduces by almost one-half the food intake of the cafeteria animals, which nevertheless remains significantly higher than that of the controls. When the injection is given at the onset of the dark period it still does not modify the intake of the controls, and it also reduces the intake of the cafeteria rats, but this time in such a way that it suppresses the hyperphagia completely and leaves the intake at a level similar to that of the controls. Comparison of "light" and "dark" intakes shows that, without naltrexone, the control animals eat twice as much during the first three hours of darkness as they do during the first three hours of light, which is the classical phenomenon for which Le Magnen has analyzed the mechanisms; with naltrexone the difference between "light" and "dark" intakes for the control animals is even greater. But for the cafeteria animals, both with and without naltrexone, the "light" intake is not significantly smaller than the "dark" intake. Thus it seems that the hyperphagic responsiveness to a vast choice of highly palatable items follows a temporal pattern different from the hunger-satiation controlled food intake of monotonous food. Such an independent rhythm should be compared to the circadian rhythm in B endorphins previously described by Fredrickson, Burgus, and Edwards (1977) using responsiveness to nociceptive stimuli and hyperalgesic activity of another opiate antagonist, naloxone. The difference in phase between the hunger-satiation loop and the ingestive behavior in response to a choice of highly palatable items has to be demonstrated in man, but one can imagine on the basis of clinical observations that the overlap between the two triggers is even greater in our species. Body fat control and obesity Barbara J. Rolls, E. T. Rolls, and E. A. Rowe Department of Experimental Psychology, University of Oxford, Oxford, 0X1 3UD, England We wish to consider the extent to which Le Magnen's (1981) interesting results and theory are applicable to the problem of obesity. Le Magnen's claim that total body energy stores are maintained at a relatively constant level ignores the fact that in many Western societies a large portion of the population does not manage to maintain a normal or even healthy level of body fat and becomes obese. Only a small number of individuals manage, once obese, to revert to normal levels of body fat. If there is a liporegulatory mechanism, then the prevalence of obesity leads us to inquire whether a large number of individuals have some defect in this system, either of energy intake or expenditure. Another possibility is that factors that control food intake and body weight can be overridden by such environmental considerations as the variety and palatability of the available food, habits, and social situations. If obesity develops following such overeating, there may be metabolic or endocrine changes that modify the liporegulatory system. We would like to challenge Le Magnen to extend his theories to cope more Table 1 (Apfelbaum & Mandenoff). Effects of Naltrexone on food intake of cafeteria and control rats during the first 3 hours of dark and light periods Light Dark Light/dark Control injection 6.32 ± 11.36 ± P< I. P. 3.42 5.16 0.025 Control