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

催乳素释放肽(PrRP)是在延髓去甲肾上腺素能神经元中合成的。我们以前已经证明，外周饱足信号八肽缩胆囊素(CCK)和应激刺激都能激活延髓去甲肾上腺素能神经元。本研究的目的是探讨PrRP在控制食物摄取和应激反应中的作用。我们首先研究了食物摄入是否激活了延髓中的PrRP神经元。CCK后PrRP神经元表达pCREB的百分比增加，提示摄食激活了PrRP神经元。给予和-PrRP中和抗体增加了每餐的食物摄入量，但不增加进餐频率，结果是增加了每天的总食物摄入量。这些数据表明，PrRP是介导CCK外周饱足信号的中枢性饱腹感因子。然后，我们研究了PrRP在情绪行为控制中的作用。给予PrRP可增加进入开放双臂的次数和在高架加迷宫测试开放目标中停留的百分比，这表明PrRP具有抗焦虑作用。给予抗PrRP中和抗体则相反，提示内源性PrRP具有抗焦虑作用。所有这些数据都与一种观点一致，即食物摄入会激活PrRP神经元，结果是停止进食并减少与焦虑相关的行为。

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.