【摘要】：焦慮癥是最為廣泛流行的精神失調(diào)癥之一,前額葉皮層和杏仁核的γ-氨基丁酸、五羥色胺和谷氨酸能系統(tǒng)的功能缺陷被認(rèn)為與焦慮癥的發(fā)病機(jī)制有關(guān)。但是在這些區(qū)域,細(xì)胞網(wǎng)絡(luò)和突觸的病理性改變及涉及的機(jī)制目前尚不清楚。 長久以來的觀點認(rèn)為五羥色胺能和γ-氨基丁酸能的突觸功能缺陷與焦慮癥相關(guān)。選擇性的五羥色胺重攝取抑制劑和γ-氨基丁酸受體增強(qiáng)劑被用來作為抗焦慮藥物使用。但是由于副作用眾多,這些藥物的治療效果需要被重新評估。最近的結(jié)果顯示,谷氨酸能系統(tǒng)也與焦慮癥有關(guān),離子型谷氨酸受體拮抗劑被認(rèn)為是潛在的抗焦慮藥物。從這個意義上講,離子型谷氨酸受體激動劑理論上可以引起小鼠的焦慮樣行為。本文闡述了離子型谷氨酸受體激動劑在焦慮癥病理性改變中的作用及其相關(guān)機(jī)制,為焦慮癥的治療提供了潛在靶點。 我們發(fā)現(xiàn),離子型谷氨酸受體激活劑海人藻酸(Kainic Acid, KA)能夠引起小鼠的焦慮樣行為,并且前邊緣皮層興奮性神經(jīng)元興奮性突觸的功能和結(jié)構(gòu)都發(fā)生了病理性改變,使用蛋白激酶C選擇性拮抗劑白屈菜紅堿(Chelerythrine Chloride, CHE)能夠阻斷雜交小鼠因為海人藻酸引起的行為、突觸功能及突觸結(jié)構(gòu)的變化。以上研究闡明了離子型谷氨酸受體激動劑在焦慮癥的發(fā)病及病理性功能和結(jié)構(gòu)改變的過程中的作用,而蛋白激酶C (Protein Kinase C, PKC)在此扮演了重要且必需的角色,為焦慮癥的治療提供了可能的研究策略和潛在的藥物靶點。
[Abstract]:Anxiety disorder is one of the most prevalent mental disorders. The functional defects of 緯-aminobutyric acid, serotonin and glutaminergic system in the prefrontal cortex and amygdala are thought to be related to the pathogenesis of anxiety disorder. However, the pathological changes in cellular networks and synapses and the mechanisms involved in these regions are unclear. It has long been argued that synaptic deficits in serotonin and 緯-aminobutyric acid are associated with anxiety disorders. Selective serotonin reuptake inhibitors and 緯-aminobutyric acid receptor enhancers are used as antianxiety drugs. But because of the many side effects, the efficacy of these drugs needs to be reassessed. Recent results suggest that glutaminergic systems are also associated with anxiety disorders, and ionic glutamate receptor antagonists are considered potential antianxiety drugs. In this sense, ionic glutamate receptor agonists can theoretically induce anxiety-like behavior in mice. This paper describes the role of ionic glutamate receptor agonists in the pathological changes of anxiety disorder and its related mechanism, which provides a potential target for the treatment of anxiety disorder. We found that the ionized glutamate receptor activator, kainic acid (Kainic Acid, KA), could induce anxiety like behavior in mice, and the function and structure of excitatory synapses in the excitatory neurons of the anterior marginal cortex had been changed pathologically. The use of (Chelerythrine Chloride, CHE), a selective protein kinase C antagonist, could block the changes in behavior, synaptic function and synaptic structure induced by kainic acid in hybrid mice. These studies illustrate the role of ionic glutamate receptor agonists in the pathogenesis of anxiety disorders and the pathological function and structural changes in which protein kinase C (Protein Kinase C, PKC) plays an important and necessary role. It provides possible research strategies and potential drug targets for the treatment of anxiety disorder.
【學(xué)位授予單位】：中國科學(xué)技術(shù)大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2014
【分類號】：R749.72

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