| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2003: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Research Abstract |
Stressful stimuli increase or decrease food intake dependent upon the stimuli applied. Neural mechanisms underling this stress-induced modulation of food intake remain to be clarified. Firstly, we attempted to make up a new instrument for measuring food intake automatically. By using this instrument, we have found that noxious stimuli with relatively weak intensity increase food intake, while emotional stimuli (immobilization stress) decrease food intake. In order to investigate neural pathways involved in stress-induced modulation, we performed a retrograde tracing study combined with Fos immunohistochemical detection. Noxious stimuli that are orexigenic stimuli activated orexin neurones in the lateral hypothalamus, which have facilitative effects upon food intake. On the other hand, anorexigenic stressful stimuli (conditioned fear stimuli) activated A2 noradrenergic neurones in the dorsomedial medulla oblongata, which contain an anorexic peptide, PrRP. Blocking of endogenous PrRP by application of anti-PrRP antibodies increased basal food intake and fasting-induced food intake, and reduced the stress-induced decrease in food intake. All these data suggest that noxious stimuli induce food intake via activation of orexin neurones, while emotional stimuli reduce food intake via activation of PrRP neurones.
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