Neural mechanisms controlling food intake during stress

压力刺激增加或减少食物摄入取决于所施加的刺激。这种应激诱导的食物摄入调节的神经机制仍有待阐明。首先，我们尝试制作一种新的自动测量进食量的仪器。通过该仪器，我们发现相对弱强度的有害刺激增加了食物摄入，而情绪刺激（固定压力）减少了食物摄入。为了研究参与应激诱导调节的神经通路，我们进行了逆行示踪研究，并结合Fos免疫组织化学检测。有害的促食刺激激活了下丘脑外侧的促食素神经元，对食物摄入有促进作用。另一方面，厌食应激刺激（条件性恐惧刺激）激活延髓后内侧A2去肾上腺素能神经元，该神经元含有厌食肽PrRP。应用抗PrRP抗体阻断内源性PrRP，增加基础摄食量和禁食诱导的摄食量，减少应激诱导的摄食量减少。所有这些数据都表明，有害刺激通过激活食欲素神经元来诱导食物摄入，而情绪刺激通过激活PrRP神经元来减少食物摄入。

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.