腺核■可抑制囓齒動物夜間攝食與食物剝奪後的攝食行為與心血管功能。首先我們在食物剝奪24小時的大白鼠由周邊注射腺核■後，再度印證100 mg/Kg 的腺核?的確可抑制攝食量(p<0.001)，並測得血漿纖瘦素與血糖亦受高劑量的腺核■作用而顯著增加。利用cFos表現量來代表中樞神經系統神經元的活性，探討腺核■在中樞作用的位置以及攝食型態的影響，結果發現攝食型態與腺核■劑量皆有顯著效果，不論在食物剝奪或自由進食之動物，腺核■可使下視丘視上核cFos總表現量顯著上升；而室旁核與弓狀核則只有在自由進食組有顯著表現增加。仔細分析各個神經元cFos表現的程度，則發現攝食型態對血管加壓素細胞具有單純主要效果，而不論事先是否剝奪食物，腺核■處理下可顯著增加視上核之催產素與血管加壓素神經元的cFos表現，但室旁核則只有催產素神經元cFos表現增加 (p<0.01)。此外，A2/C2及A14兒茶酚胺細胞之cFos表現亦受攝食型態影響，而靜脈注射高劑量的腺核■會使A1/C1、A6與A14兒茶酚胺神經元的cFos表現量增加 (p<0.01)，A2/C2、A12則沒有顯著差異。研究的神經組織中A1/C1、A6的兒茶酚胺細胞群以及視上核之血管加壓素細胞，可隨靜脈給予的腺核■劑量增加而增加cFos表現；此現象與腺核■抑制心血管功能的影響相似。而在食物剝奪動物中催產素與A14神經元cFos的表現，則只在高劑量的腺核■作用下有顯著增加，此和腺核■所引起的抑制攝食行為之結果相仿；這些結果暗示著造成抑制攝食行為的改變可能與中樞神經系統催產素與兒茶酚胺細胞有一定的相關性。; Adenosine is a potent inhibitor of cardiovascular function and also suppresses normal nocturnal and food deprivation-induced food intake. First, my study confirmed that peripheral injection of 100 mg/Kg adenosine was able to inhibit food intake in animals fasted for 24hr (P<0.001). Analysis of blood samples revealed that plasma leptin and glucose concentrations were significantly elevated by 100 mg/Kg of adenosine. In the present study, cFos expression was used to investigate possible sites of the central nervous system that may be involved in the anoretic effect of adenosine. The effect of previous feeding pattern on the expression of cFos was also studied. Ad libitum fed (AF) or food deprived (FF) conscious male rats received an intravenous injection of adenosine (0, 10 or 100 mg/Kg) and then were sacrificed 2h later. Brain sections were subjected to immunocytochemistry of cFos and oxytocin (OT)、vasopressin (VP) or tyrosine hydroxylase (TH). Statistical analysis revealed that both feeding pattern and adenosine had main effects on total cFos expression in the hypothalamus. In the supraoptic nucleus (SON) of the hypothalamus there was an increase of overall cFos immunoreactivity in FF and AF rats. But cFos expression in the paraventricular nucleus (PVN) and arcuate nucleus (ARC) were significantly increased only in AF rats. cFos expression in VP but not OT neurons was also affected by feeding pattern. In SON, cFos expression in both OT and VP neurons was enhanced by adenosine treatment, suggesting that these neurons were activated. On the other hand, OT but not VP neurons in PVN were also activated by adenosine. In addition, intravenous injection of adenosine increased cFos expression in A1/C1, A6 and A14 catecholaminergic neurons but not in A2/C2 or A12. There was a main effect of feeding pattern on cFos expression in A2/C2 and A14. Both adenosine-induced vasodilation and cFos expression in brain stem catecolaminergic neurons and hypothalamic VP neurons followed a dose-dependent pattern, suggesting that these neurons may be more closely related to the cardiovascular function. However, cFos activity in oxytocinergic neurons and A14 in the hypothalamus was increased only by 100 mg/Kg adenosine, the only dose that was effective in suppressing food intake. The results suggest that anoretic effect of adenosine is probably associated with activation of oxytocinergic and specific catecholaminergic neurons in the central nervous system.
