| Project/Area Number |
18590223
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | Jichi Medical University |
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Principal Investigator |
ONAKA Tatsushi Jichi Medical University, School of Medicine, Professor (90177254)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,860,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥360,000)
Fiscal Year 2007: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2006: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Food Intake / Stress / PrRP / Noradrenaline / CCK / Satiet / コレシストキニン / プロクラチン放出ペプチド / ストレス / 視床下部 / ノルアドレナリン / PrRP / 満腹 / 孤束路核 |
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| Research Abstract |
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.
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