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  本文關(guān)鍵詞： 電生理 nesfatin-1 迷走神經(jīng)復合體(DVC) 葡萄糖敏感神經(jīng)元 攝食　出處：《青島大學》2010年碩士論文　論文類型：學位論文

【摘要】： Nesfatin-1是一個由82個氨基酸組成的多肽,側(cè)腦室注射后可以抑制攝食,nesfatin-1是其中一個分泌片段,其前體蛋白nucleobindin2(NUCB2)經(jīng)過激素轉(zhuǎn)化酶的裂解作用生成三個片段,一個N端片段(nesfatin-1)和兩個C端片段(nesfatin-2和nesfatin-3)。1側(cè)腦室注射nesfatin-1有抑制攝食的作用并且呈現(xiàn)劑量依賴效應(yīng),注射其抗體后攝食增加。然而側(cè)腦室注射nesfatin-2和nesfatin-3并不能增強飽感,因而NUCB2只有轉(zhuǎn)化為nesfatin-1才能起到抑制攝食的作用。長期側(cè)腦室注射nesfatin-1可以使體重減輕,而長期注射其抗體則使體重增加。在leptin受體突變的大鼠nesfatin-1可以使攝食減少,注射nesfatin-1的抗體并不能阻斷l(xiāng)eptin導致的攝食減少。這可以說明NUCB2是非依賴leptin的飽食分子。另外中樞注射α-MSH可以使NUCB2基因在室旁核表達增加,并且由nesfatin-1引起的飽食作用可以被α-MSH受體的拮抗劑所拮抗。所以我們認為nesfatin-1抑制攝食的作用機制與下丘腦的促黑激素信號系統(tǒng)有關(guān)。 目的觀察nesfatin-1對大鼠迷走神經(jīng)復合體(dorsal vagal complex, DVC)胃擴張敏感神經(jīng)元和葡萄糖感受神經(jīng)元放電頻率的調(diào)制作用,探討其參與攝食調(diào)控的可能機制。觀察DVC注射nesfatin-1對攝食的影響 方法1)采用多管玻璃微電極記錄單個細胞單位放電的電生理學方法,觀察大鼠DVC區(qū)微量注射nesfatin-1前后上述兩種神經(jīng)元放電頻率的變化,以微量注射0.9% NaCl作對照。2)采用行為學方法觀察DVC區(qū)微量注射nesfatin-1前后攝食量和體重的變化。以微量注射0.9% NaCl作對照。 結(jié)果1)在DVC中記錄到的109個神經(jīng)元經(jīng)多管微電極給予葡萄糖,有46個放電頻率降低(鑒定為G-INH);31個放電頻率升高(鑒定為G-EXC);32個對葡萄糖沒有反應(yīng)。在39個G-INH經(jīng)多管微電極給予nesfatin-1,有33個神經(jīng)元放電頻率降低,1個放電頻率升高,5個對nesfatin-1無反應(yīng)。在26個G-EXC神經(jīng)元中,有20個放電頻率升高,3個神經(jīng)元放電頻率降低,3個對nesfatin-1無反應(yīng)。 2)在DVC中記錄到89個神經(jīng)元對其進行胃擴張(GD)刺激,48個神經(jīng)元被激活(鑒定為GD-EXC),21個神經(jīng)元被抑制(鑒定為GD-INH),其余20個神經(jīng)元對胃擴張無反應(yīng)。在42個GD-EXC神經(jīng)元,其中32個被nesfatin-1所興奮,10個對nesfatin-1無反應(yīng)。在18個GD-INH神經(jīng)元,16個被nesfatin-1所抑制,2個無反應(yīng)。上述兩類神經(jīng)元經(jīng)多管微電極給予0.9%NaCl,注射前后神經(jīng)元放電頻率的變化無統(tǒng)計學意義。 3)DVC內(nèi)微量注射nesfatin-1后攝食量減少,體重減輕。 結(jié)論Nesfatin-1能夠調(diào)制DVC胃擴張敏感神經(jīng)元和葡萄糖感受神經(jīng)元的興奮性,可以使大鼠攝食減少,體重減輕。這可能是nesfatin-1抑制攝食的部分機制。
[Abstract]:Nesfatin-1 is a peptide composed of 82 amino acids, which can be inhibited by intracerebroventricular injection. The precursor protein nucleobindin2nu CB2 (nucleobindin2nu CB2) is one of the secretory fragments, which can be divided into three fragments by glucocorticoid converting enzyme cleavage. One N-terminal fragment, one N-terminal fragment, and two C-terminal fragments, nesfatin-1, and two C-terminal fragments, nesfatin-1 injection into the lateral ventricle of nesfatin-3).1, had a dose-dependent effect on the inhibition of food intake. However, the injection of nesfatin-2 and nesfatin-3 into the lateral ventricle could not enhance the satiety. Long term intraventricular injection of nesfatin-1 can reduce body weight, while long term injection of its antibody can result in weight gain. In rats with leptin receptor mutation, nesfatin-1 can reduce food intake. The antibody injected with nesfatin-1 could not block the decrease of food intake induced by leptin, which indicated that NUCB2 was not dependent on leptin. In addition, 偽 -MSH could increase the expression of NUCB2 gene in paraventricular nucleus after central injection of 偽 -MSH. The satiety induced by nesfatin-1 can be antagonized by 偽 -MSH receptor antagonist. Therefore, we think that the mechanism of nesfatin-1 inhibiting feeding is related to the signal system of melanotropic hormone in hypothalamus. Objective to observe the modulating effect of nesfatin-1 on the frequency of gastric dilatation sensitive neurons and glucose-sensing neurons in rat vagal complex vagal complex (DVCs), and to explore the possible mechanism of its involvement in the regulation of feeding. To observe the effect of DVC injection of nesfatin-1 on feeding. Methods 1) the electrophysiological method of recording single cell unit discharge with multi-tube glass microelectrode was used to observe the changes of discharge frequency of the two neurons before and after microinjection of nesfatin-1 into the DVC region of rats. The changes of food intake and body weight before and after microinjection of nesfatin-1 in DVC area were observed by using microinjection of 0.9% NaCl as control group, and 0.9% NaCl as control. Results 1) 109 neurons recorded in DVC were given glucose via multi-tube microelectrode. Forty-six discharges decreased (identified as G-INHN; 31 increased (identified as G-EXCN; 32 were not responsive to glucose). In 39 G-INH treated with multitube microelectrode, the discharge frequency of 33 neurons decreased and 1 increased. In 26 G-EXC neurons, The discharges were increased in 20 neurons, decreased in 3 neurons, and showed no response to nesfatin-1 in 3 neurons. 2) 89 neurons were recorded in DVC stimulated by gastric dilatation, 48 neurons were activated (identified as GD-EXCN, 21 neurons were inhibited (identified as GD-INHN), the remaining 20 neurons were not responsive to gastric dilatation. 32 of them were excited by nesfatin-1, 10 did not respond to nesfatin-1, 18 GD-INH neurons were inhibited by nesfatin-1, 16 neurons were inhibited by nesfatin-1, and 2 neurons were not reacted. The two types of neurons were given 0.9g Na Cll with multiple microelectrodes. There was no significant difference in the frequency of neuronal discharge before and after injection. After microinjection of nesfatin-1, the food intake decreased and the body weight decreased. Conclusion Nesfatin-1 can modulate the excitability of DVC gastric dilatation sensitive neurons and glucose-sensing neurons, which may be the mechanism of nesfatin-1 inhibiting feeding.
【學位授予單位】：青島大學
【學位級別】：碩士
【學位授予年份】：2010
【分類號】：R338.2

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相關(guān)期刊論文 前1條

1 張曉紅;陳曦;蔣正堯;;α-MSH對大鼠背側(cè)迷走神經(jīng)復合體胃擴張敏感神經(jīng)元的作用[J];青島大學醫(yī)學院學報;2009年03期

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本文編號：1528808