Role of PrRP neurons in the control of food intake and emotional responses

催乳素释放肽（Prolactin-releasing peptide，PrRP）在延髓的去甲肾上腺素能神经元中合成。我们以前已经表明，无论是外周饱腹信号，八肽胆囊收缩素（CCK）和应激刺激激活去甲肾上腺素能神经元在延髓本研究的目的是调查的角色PrRP在控制的食物摄入和应激反应。我们首先研究了食物摄入是否激活延髓中的PrRP神经元。CCK后PrRP神经元表达pCREB的百分比增加，表明食物摄入激活PrRP神经元。施用and-PrRP中和抗体增加了每餐的食物摄入量，但没有增加用餐频率，因此，增加了每天的食物摄入总量。这些数据表明，PrRP是一个中枢性的饱腹感因子，它介导CCK的外周饱腹感信号。PrRP的管理增加了进入开放臂的数量和高架十字迷宫测试的开放目标中的停留百分比，表明PrRP具有抗焦虑作用。施用抗PrRP中和抗体具有相反的效果，表明内源性PrRP具有抗焦虑作用。所有这些数据都与食物摄入激活PrRP神经元的想法一致，因此停止进食并减少焦虑相关行为。

Prolactin-releasing peptide (PrRP) is synthesized in the noradrenergic neurons of the medulla oblongata. We have previously shown that both a peripheral satiety signal, cholecystokinin octapeptide (CCK) and stressful stimuli activate noradrenergic neurons in the medulla oblongata The aim of this study is to investigate roles of PrRP in the control of food intake and stress responses. We firstly examined whether food intake activates PrRP neurons in the medulla oblongata. The percentage of PrRP neurons expressing pCREB was increased following CCK, suggesting that food intake activates PrRP neurons. Administration of and-PrRP neutralizing antibodies increased the amount of food intake per meal but not the meal frequency, as a result, increased the total amount of food intake per day. The data suggest that PrRP is a central satiety factor that mediates peripheral satiety signaling of CCK We then examined whether effects of PrRP in the control of emotional behavior. Administration of PrRP increased the number of entries into the open arms and the percentage of stay in the open aims of an elevated plus maze test, suggesting that PrRP has anxiolytic effects. Administration of anti-PrRP neutralizing antibodies had the opposite effects, suggesting that endogenous PrRP has anxiolytic actions. All these data are consistent with an idea that food intake activates PrRP neurons, as a result stops eating and reduces anxiety-related behavior.