Sucrose modifies c-fos mRNA expression in the brain of rats maintained on feeding schedules.

Food intake is regulated according to circadian activity, metabolic needs and the hedonic value of food. Rodents placed on a fixed feeding schedule show behavioral and physiological anticipation of mealtime referred to as food-anticipatory activity (FAA). FAA is driven by the food-entrainable oscillator (FEO), whose anatomical substrate is not yet known. Recent data have shown that restricted feeding schedules for regular chow and daily limited access to palatable food in free-feeding rats activate distinct brain regions during FAA. The combination of a deprivation regimen and scheduled access to palatable food may give rise to a more global anticipatory mechanism because the temporal cycles of energy balance would be strongly modulated by the incentive properties of palatable food; however, the neuronal response to this combined treatment is not yet known. The present study investigated how adding palatable sucrose to feeding schedules affects the pattern of brain c-fos mRNA expression during FAA (0-3 h) and 1 h following feeding. The rats maintained on scheduled chow access increased their daily chow intake, while the rats maintained on scheduled sucrose and chow mainly increased their daily sucrose intake. Adding sucrose to scheduled feeding displaced c-fos mRNA expression from the dorsomedial and paraventricular hypothalamic nuclei and posterior lateral hypothalamus (LH) to the prefrontal cortex, lateral septum, nucleus accumbens and anterior LH. During refeeding, the rats on scheduled sucrose demonstrated higher activation of the nucleus of the solitary tract. The present results suggest that palatable sucrose combined with restricted feeding schedules activate a distinct neuronal network compared to neuronal activation produced by scheduled access to regular chow. These data provide evidence that the brain may contain different food-oscillatory systems and that food palatability may shift the neuronal activity from the medial hypothalamus to the limbic and reward-related areas even at the negative metabolic state.