Neural mechanisms of anti-stress effects of food intake

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Neural mechanisms of anti-stress effects of food intake were investigated.1 Roles of PrRP (prolactin-releasing factor) in food intake and stress responsesPrRP neurons are activated by the peripheral satiety factor, CCK. PrRP induces release of stress hormones, ACTH, vasopressin and oxytocin. We thus examined roles of PrRP in satiety and stress responses in rats. Neutralization of endogenous PrRP with antibodies increased amounts of food intake per meal. An icv injection of PrRP attenuated anxiety-related behaviour in an elevated plus maze test, while neutralization of endogenous PrRP augmented anxiety behavior. Neutralization of endogenous PrRP attenuated expression of Fos protein in the hypothalamic paraventricular nuclei, and oxytocin release in response to stressful stimuli. All these data suggest that PrRP plays an important role in satiety and stress responses after food intake.2.Roles of leptin and ghrelin in stress responsesFood intake increases plasma leptin and decreases ghrelin concentrations. We examined effects of leptin and ghrelin in noradrenaline release in the hypothalamus and plasma ACTH concentrations after stressful stimuli. Leptin attenuated increases in noradrenaline release in the hypothalamus and plasma ACTH concentrations following stressful stimuli, while ghrelin augmented these increases. These data suggest that leptin and ghrelin also play important roles in anti-stress effects of food intake.3.Roles of salt intake in stress responsesStress increases salt intake. We thus examined hyperosmotic stimuli upon stressful responses. An increase in plasma osmolality attenuated increases in noradrenaline release in the hypothalamus and plasma ACTH concentrations following stressful stimuli. These data suggest that salt intake plays an inhibitory role in stress responses.All these data suggest that PrRP, leptin, ghrelin and plasma osmolality play important roles in anti-stress effects of food intake.