動情激素對腺核■抑制攝食行為與 對神經胜■神經元活性之影響; Effect of estrogen on adenosine-induced anorexia and neuropeptide neuronal activities.

CMUR > College of Medicine > Graduate Institute of Medical Science > Theses & dissertations > Item 310903500/23997

Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/23997

Title:	動情激素對腺核■抑制攝食行為與對神經胜■神經元活性之影響;Effect of estrogen on adenosine-induced anorexia and neuropeptide neuronal activities.
Authors:	陳貴米;Kuei-Mi Chen
Contributors:	中國醫藥學院醫學研究所
Keywords:	雌二醇;腺核;攝食;血壓;心跳;神經胜;一氧化氮;下視丘;17β-estradiol;adenosine;food intake;blood pressure;heart rate;neuropeptide;nicotinamide adenine dinucleotide phosphate- diapharase;hypothalamus
Date:	1999
Issue Date:	2009-12-02 14:11:35 (UTC+8)
Abstract:	腺核■ (Adenosine) 屬於一種嘌呤類核■ (Purine nucleoside)，可使血管舒張、肌肉鬆弛與減少動物攝食行為。而本實驗即要探討動情激素是否會調節腺核■抑制攝食行為及心血管功能之作用。本研究採用動情激素或芝麻油處理之卵巢切除的雌性大白鼠，並於食物剝奪24小時後，由皮下注射各種劑量之腺核■（saline, 10, 100 mg/Kg），結果顯示，高劑量腺核■ (100 mg/Kg) 會抑制攝食行為，但只在恢復攝食2小時內有效，而在動情激素的作用下，於8小時後總進食量會代償至對照組之水準。於相同處理之卵巢切除的雌性大白鼠，測量股靜脈注射腺核■（saline, 5, 10, 50, 100 mg/Kg）後對血壓與心跳速率之影響。結果顯示，各劑量之腺核■皆會降低血壓與心跳速率，而動情激素則可減緩心跳之下降幅度及加速心跳恢復正常，且動情激素對腺核■所引起之降低血壓作用亦有類似之影響。由此實驗推論，動情激素具有調節心血管的功能。免疫組織化學染色結果顯示，注射腺核■會使視上核cFos的表現量增加 (P<0.01)，且有劑量依賴（dose-dependent）的關係，但在室旁核則無顯著差異。而腺核■會增加視上核與室旁核催產激素神經細胞表現cFos，但血管加壓素神經細胞中cFos表現只於視上核有顯著的變化。藉此推測，腺核■在下視丘以活化催產激素神經細胞為主，而動情激素並不會影響cFos的表現。除此之外，動情激素亦不影響下視丘或大腦皮質的NADPH去氫■、催產激素、神經胜■Y與血管加壓素的表現。本研究顯示，動情激素並不會影響腺核■所引起的cFos表現與厭食反應，但對長期之體重控制與心血管功能具有調節作用，而此現象並非因影響催產激素、血管加壓素、神經胜■Y或NADPH去氫■神經細胞所產生的。; Adenosine induces vasodilatation, muscle relaxation and anorexia in animals. To investigate whether the anoretic effect of adenosine is modulated by estrogen, adult ovariectomized (OVX) rats primed with either estradiol (E2, 10μg/rat) or sesame oil (OIL) were deprived of food for 24h and subjected to peripheral adenosine injection (0, 10, 100 mg/kg) immediately prior to refeeding. The results showed that administration of 100 mg/kg adenosine reduced food intake at the first two hour of refeeding regradless of the steroid milieu of the rats, even though E2- primed rats had leaner body size. However, in E2-treated rats, this initial supression of food intake was compensated by 8h of refeeding, whereas in OVX+OIL animals cumulated food intake at the same time point was still significantly lower than that of saline-injected rats. I then investigated whether E2 could modulate the hypotensive and bradycardiac effects of adenosine by measuring blood pressure and heart rate in anesthetized OVX rats that had been treated with either estradiol (E2, 10μg/rat) or sesame oil for 2 days. Blood pressure and heart rate were significantly suppressed by every adenosine dose administered (P<0.0001). Statistic analysis revealed a main effect of E2 on heart rate (P=0.0002) and duration of bradycardia (P=0.0001). E2 also reduced the hypotensive response to adenosine. These data suggest that E2 can modulate adenosine-induced inhibition of cardiovascular functions in female rats. Immunohistochemical staining showed increased cFos expression in supraoptic nucleus (SON) after adenosine injection in a dose-dependent manner but not in paraventricular nucleus (PVN). cFos expression in oxytocin (OT) neurons in both PVN and SON and in vasopressin (VP) neurons in SON was also increased by adenosine, suggesting that adenosine preferentially activated OT neurons. However, E2 failed to have an impact on the induction of cFos. Expression of OT, VP, neuropeptide Y (NPY) and NADPH-diaphorase (NADPH-d) in the hypothalamus or cerebral cortex was not affected by estrogen either. The data indicated that although adenosine-induced anorexia or cFos expression in the central nervous system was not influenced by E2, E2 did play a modulatory role in the long-term control of body weight and food intake and in cardiovascular responses to adenosine. Nevertheless, these effects of E2 were unlikely mediated by hypothalamic OT, VP, NPY or NADPH-d neurons.
Appears in Collections:	[Graduate Institute of Medical Science] Theses & dissertations

Files in This Item:

File	Description	Size	Format
index.html		0Kb	HTML	208	View/Open

Loading...