本文選題：糖皮質(zhì)激素 + 抑郁癥�。� 參考：《青島大學(xué)》2017年碩士論文

【摘要】：目的:探討糖皮質(zhì)激素是如何影響杏仁核亞細(xì)胞結(jié)構(gòu)及興奮性神經(jīng)元和抑制性神經(jīng)元之間的相互作用的影響及其機(jī)制,或許能夠揭示制度抑郁癥及焦慮的病理機(jī)制。方法:地塞米松對(duì)于神經(jīng)元的作用是通過(guò)把地塞米松急性洗在杏仁核腦片上或者直接給小鼠腹腔注射兩種方式進(jìn)行探討。用700B放大器在電壓鉗下記錄突觸興奮性,在電流鉗下記錄細(xì)胞細(xì)胞自身特性。GABA能神經(jīng)元的功能的研究通過(guò)記錄自身興奮性以及抑制性輸出來(lái)表示,谷氨酸能神經(jīng)元功能的研究通過(guò)記錄自身興奮性及興奮性輸出來(lái)表示,杏仁核神經(jīng)元?jiǎng)幼麟娢话l(fā)放能力通過(guò)注入去極化電流來(lái)研究。以谷氨酸能神經(jīng)元被黃色熒光蛋白標(biāo)記、GABA能神經(jīng)元被綠色熒光蛋白標(biāo)記的轉(zhuǎn)基因小鼠的杏仁核為研究對(duì)象,通過(guò)一天一次慢性注射(40mg/kg)一周地塞米松及地塞米松(25μM)急性洗在腦片上兩種方式,運(yùn)用全細(xì)胞膜片鉗,通過(guò)記錄在谷氨酸能神經(jīng)元記錄自發(fā)抑制性突觸后電位(spontaneous inhibitory postsynaptic current,s IPSC)、動(dòng)作電位時(shí)間間隔(inter spike intervals,ISI)及在GABA能神經(jīng)元記錄自發(fā)興奮性突觸后電位(spontaneous excitatory postsynaptic current,s EPSC)、動(dòng)作電位時(shí)間間隔(inter spike intervals,ISI)反應(yīng)神經(jīng)元的動(dòng)作電位和突觸傳遞,探討糖皮質(zhì)激素對(duì)于杏仁核亞細(xì)胞結(jié)構(gòu)和神經(jīng)元相互作用網(wǎng)絡(luò)的影響。結(jié)果:慢性應(yīng)用地塞米松增加抑制性神經(jīng)元GABA能神經(jīng)遞質(zhì)的釋放,并且增加興奮性神經(jīng)元上GABAA受體的反應(yīng)性。急性應(yīng)用地塞米松能夠增加抑制性神經(jīng)元GABA神經(jīng)遞質(zhì)的釋放,對(duì)GABAA受體反應(yīng)性沒(méi)有明顯影響。急性和慢性應(yīng)用地塞米松都能增加GABA能神經(jīng)元?jiǎng)幼麟娢坏陌l(fā)放能力,增加細(xì)胞自身興奮性。慢性應(yīng)用地塞米松能夠下調(diào)興奮性神經(jīng)元釋放谷氨酸能神經(jīng)遞質(zhì),并且急性應(yīng)用地塞米松也能下調(diào)興奮性神經(jīng)元谷氨酸能神經(jīng)遞質(zhì)的釋放。急性和慢性應(yīng)用地塞米松對(duì)谷氨酸能神經(jīng)元?jiǎng)幼麟娢话l(fā)放能力沒(méi)有明顯影響。應(yīng)用地塞米松對(duì)于杏仁核抑制性神經(jīng)元和興奮性神經(jīng)元產(chǎn)生不同的作用,急性和慢性應(yīng)用地塞米松都會(huì)上調(diào)GABA能神經(jīng)元的遞質(zhì)釋放和動(dòng)作電位發(fā)放能力以及下調(diào)谷氨酸能的遞質(zhì)釋放,慢性應(yīng)用地塞米松也會(huì)增加GABA受體的反應(yīng)性。結(jié)論:地塞米松通過(guò)提高突觸前神經(jīng)元活性、GABA能神經(jīng)元的釋放以及突觸后GABAA受體的反應(yīng)性上調(diào)GABA能神經(jīng)元對(duì)于谷氨酸能神經(jīng)元的作用;通過(guò)降低谷氨酸能神經(jīng)遞質(zhì)的釋放降低谷氨酸能神經(jīng)元對(duì)于GABA能神經(jīng)元的作用。杏仁核谷氨酸能神經(jīng)元功能的下調(diào)與GABA能神經(jīng)元的上調(diào)與損傷了神經(jīng)網(wǎng)絡(luò)的平衡,這種對(duì)于處于抑制狀態(tài)的杏仁核神經(jīng)網(wǎng)絡(luò)調(diào)節(jié)的不協(xié)調(diào)或許導(dǎo)致應(yīng)激狀態(tài)的情緒情感障礙,為抗抑郁藥物開發(fā)提供新思路。
[Abstract]:Objective: To explore the effect of glucocorticoid on the interaction between the amygdala subcellular structure and the interaction between excitatory and inhibitory neurons, and perhaps to reveal the pathological mechanism of institutional depression and anxiety. Methods: Dexamethasone's effect on neurons is through the acute washing of dexamethasone in the amygdala. Two ways of intraperitoneal injection were conducted on or directly to the mice. 700B amplifier was used to record synaptic excitability under voltage forceps, and the function of cell cell itself characteristic.GABA neurons under current forceps was recorded by recording self excitability and suppressive transmission, and the function of glutamic acid neurons was studied. The action potential delivery ability of amygdala neurons was studied by injection depolarization current. The glutamic acid neurons were labeled with yellowish fluorescent protein. The apricot kernel of transgenic mice marked by green fluorescent protein (GABA) neurons was studied by a single day chronic injection. An acute wash of dexamethasone (40mg/kg) and dexamethasone (25 mu M) on the brain slices in two ways, using the whole cell patch clamp, recording the spontaneous inhibitory postsynaptic potential (spontaneous inhibitory postsynaptic current, s IPSC) by recording the glutamic acid neurons, the time interval of the action potential (inter spike intervals, ISI) and The neurons recorded the spontaneous excitatory postsynaptic potential (spontaneous excitatory postsynaptic current, s EPSC), the action potential and synaptic transmission of the action potential time interval (inter spike intervals, ISI), and the effects of glucocorticoid on the structure of the amygdala subcell and the neural interaction network. Dexamethasone increases the release of GABA neurotransmitters in inhibitory neurons and increases the responsiveness of GABAA receptors on excitatory neurons. Acute dexamethasone can increase the release of GABA neurotransmitters in the inhibitory neurons and have no significant response to the responsiveness of the GABAA receptor. Both acute and chronic use of dexamethasone can increase G ABA can increase the ability of neuronal action potential to increase cell self excitability. Chronic dexamethasone can reduce the release of glutamatergic neurotransmitters from excitatory neurons, and acute dexamethasone can also reduce the release of glutamate neurotransmitters in excitatory neurons. Acute and chronic dexamethasone is capable of glutamatergic neurotransmitters The use of dexamethasone has different effects on the amygdala and the excitatory neurons in the amygdala. The acute and chronic use of dexamethasone can up-regulate the release of GABA neurons and the ability to release the action potential and reduce the release of glutamate neurotransmitters. Dexamethasone also increases the reactivity of GABA receptors. Conclusion: dexamethasone can increase the action of GABA neurons to glutamic neurons by increasing the activity of pre synapse neurons, release of GABA energy neurons and the reactivity of postsynaptic GABAA receptors, and reduce glutamatergic neurotransmitters to reduce glutamatergic neurons by reducing the release of glutamate neurotransmitters. The downregulation of the function of glutamic neurons in the amygdala and the up-regulation of the GABA energy neurons and the balance of the neural network, the incoordination of the regulation of the amygdala neural network in the state of inhibition may lead to emotional and emotional disorders in the state of stress and provide new ideas for the development of antidepressant drugs in the amygdala.
【學(xué)位授予單位】：青島大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R749.4

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