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系統識別號 U0026-1807201110011500
論文名稱(中文) 性別差異影響壓力感受度之探討:以海馬迴CA1區域長期抑制作用表現為分析指標
論文名稱(英文) Sex Differences in Stress Response: Assessing on a Stress-Induced Enhancement of Long-Term Depression Induction in the Hippocampal CA1 Region
校院名稱 成功大學
系所名稱(中) 藥理學研究所
系所名稱(英) Department of Pharmacology
學年度 99
學期 2
出版年 100
研究生(中文) 陳家鵬
研究生(英文) Jia-Peng Chen
學號 s26984074
學位類別 碩士
語文別 中文
論文頁數 76頁
口試委員 指導教授-許桂森
口試委員-郭余民
口試委員-黃阿敏
中文關鍵字 壓力  性別差異  長期抑制現象  海馬迴 
英文關鍵字 stress  sex difference  long-term depression  hippocampus 
學科別分類
中文摘要 男性與女性在大腦的 組成及行為表現上會因為性別的不同而表現出差異性。女性個體在過去的臨床統計結果發現,她們在面對壓力後所造成的情緒性疾病相較於男性個體較為敏感,而且罹患精神性疾病的機率大約為兩倍。為什麼會造成如此性別上的差異,科學家推測此等差異可能發生在下視丘-腦下垂體-腎上腺內分泌壓力反應軸上,由於性別的不同而造成因應壓力的代償性作用以及影響腦中神經傳遞物質之間的交互作用產生了差異。
我們實驗室之前的研究已經證明,急性壓力會促進成年雄性大鼠海馬迴CA1區域的長期抑制作用產生,但對於此壓力促進長期抑制作用的現象是否存在著性別的差異仍不清楚。因此,我們利用給予實驗鼠一種無法預測、無法逃脫的限制性尾巴電擊急性壓力模式,來探討此課題。實驗結果發現,以青春期週齡的雄性大鼠為實驗材料,相較於對照組的雄性大鼠,經歷急性壓力後所製備的海馬迴腦薄片,用連續低頻電刺激的方式,能促進海馬迴CA1區域的長期抑制作用形成,反觀在雌性大鼠則不明顯。我們也發現雄性大鼠的海馬迴突觸小體,在麩胺酸再吸收能力上會因為急性壓力的處理而受到抑制,但此現象在雌性大鼠則不明顯。若在對照組大鼠的腦薄片直接投予N-甲基-D-天冬胺酸(NMDA)處理或是在麩胺酸運送通道抑制劑DL -蘇-β-芐氧基天冬氨酸(DL-TBOA)存在下,並同時以連續低頻電刺激的方式誘發長期抑制作用,則不會產生性別的差異。另外,如果在經歷急性壓力後的雄性大鼠海馬迴腦薄片上,以配對性連續低頻電刺激,亦可以促進長期抑制作用。若在進行急性壓力前,將雄性大鼠兩側的腎上腺進行切除手術,則急性壓力所促進的長期抑制作用會受到抑制。除此之外,直接檢測血漿內反應壓力的皮質酮濃度變化則發現,雌性大鼠在未施予壓力前皮質酮較雄性大鼠高,然而給予壓力之後,皮質酮的濃度卻與雄性大鼠沒有太大的差異。此外,我們也發現雌性大鼠其海馬迴糖皮質酮受體的表現量較雄性大鼠少,並且在其下視丘-腦下垂體-腎上腺內分泌壓力軸負向回饋作用也較雄性大鼠差。此外,此種性別差異在將雌性大鼠卵巢切除並不會消失;反之,若將剛出生的雌性仔鼠施打睪固酮則可以在其成熟後海馬迴CA1區域誘發出壓力所促進長期抑制現象,針對這樣的結果也說明了兩性在經歷壓力後所誘發的海馬迴突觸塑性改變,係透過睪固酮於發育早期在大腦內不可逆組織化影響的結果,並且其與糖皮質酮受體的表現程度是有關的。
英文摘要 Females and males are different in both brain and behavior. Females are more susceptible than males to stress-induced affective disorders and twice as likely to experience depression. These differences are probably underlined by sexual dimorphisms observed in the hypothalamic-pituitary-adrenal (HPA) axis activity/response to stress and its interaction with the central neurotransmitter systems. Our previous studies revealed that acute stress facilitates the occurrence of long-term depression (LTD) in hippocampal CA1 area. However, it remains unknown whether sex differences exist in the effect of stress on LTD. Using an acute unpredictable and inescapable restraint tailshock stress paradigm, we report here that hippocampal slices from stressed male rats expressed larger LTD by low-frequency stimulation (LFS) than controls, whereas such effect was not observed in female rats during puberty. The facilitatory effect of stress on LTD was prevented when animals were submitted to bilateral adrenalectomy. However, no sex differences in the magnitude of LTD induced by direct application of N-methy-D-aspartate (NMDA)or a combination of LFS with the glutamate uptake inhibitor DL-threo--benzyloxyaspartate (DL-TBOA) were observed in slices from naive rats. Female rats exhibited significantly higher basal but lower stress-evoked levels of plasma corticosterone than male rats. We also found that stress induces a profound decrease in the glutamate uptake in hippocampal synaptosomal preparations from male but not female rats. The expression of hippocampal glucocorticoid receptor (GR) and GR-mediated negative feedback on the HPA axis in female rats are significantly less than those in male rats. Furthermore, hippocampal slices from stressed male but not female rats showed an increase in the induction of LTD by paired-pulse LFS. Importantly, female rats that are masculinized with testosterone at birth respond to stress like male rats do, demonstrating an enhancement of LTD. In contrast, ovariectomized female rats failed to restore the ability of stress to facilitate LTD. These results reveal an obvious sex difference in stress-induced modification of hippocampal synaptic plasticity, which depends on organizational effect of testosterone during early development and the expression levels of glucocorticoid receptors in hippocampal CA1 region.
論文目次 考試合格證明I
中文摘要(Abstract in Chinese)II
英文摘要(Abstract in English)V
誌謝VIII
目錄X
圖目錄XIII
縮寫檢索表(Abbreviations)XIV
第一章、緒論(Introduction)01
1-1. 何謂壓力 02
1-2. 壓力活化下視丘-腦下垂體-腎上腺內分泌壓力軸 03
1-3. 皮質酮結合球蛋白調控皮質酮的濃度04
1-4. 性別對於壓力反應的差異06
1-5. 壓力對於長期抑制作用的影響08
1-6. 壓力影響興奮性神經傳遞物質麩胺酸10
1-7. 發育早期組織化所造成的性別差異11
1-8. 研究目的12
第二章、材料與方法(Materials and Methods)14
2-1. 實驗動物 15
2-2. 動物藥物去勢處理15
2-3. 海馬迴腦切片製備16
2-4. 胞外電氣生理學紀錄法17
2-5. 藥物處理腦薄片記錄fEPSP18
2-6. 血中皮質類固醇檢測19
2-7. 急性壓力模式及血液收集19
2-8. 麩胺酸受體麩胺酸再攝取試驗19
2-9. 西方墨點法23
2-10. 母鼠雌激素週期檢測28
2-11. 卵巢切除手術 29
2-12. 腎上腺切除手術29
2-13. 統計分析29
第三章、實驗結果(Results)31
3-1. 急性壓力促進雄性大鼠而非雌性大鼠之海馬迴CA1區域的長期抑制作用產生 32
3-2. 壓力感受度性別上的差異與長期抑制作用的誘發機制無關33
3-3. 皮質酮參與急性壓力促進長期抑制現象誘發的作用34
3-4. 糖皮質酮受體的表現量造成性別壓力感受度的不同36
3-5. 壓力促進長期抑制作用的生成是透過睪固酮在發育早期之組織化影響37
第四章、討論(Discussion)39
4-1. 主要研究發現40
4-2. 急性壓力促進長期抑制作用表現呈現性別上之差異性40
4-3. 急性壓力造成麩胺酸再吸收之性別差異41
4-4. 下視丘-腦下垂體-腎上腺內分泌壓力軸之性別差異42
4-5. 皮質酮與皮質酮結合蛋白關係43
4-6. 性荷爾蒙與性別長期抑制作用之差異44
4-7. 糖皮質酮受體活化程度的性別差異45
4-8. 長期抑制作用在生理中扮演可能的角色47
4-9. 結論48
第五章、圖表(Figures)50
第六章、參考文獻(References)61
作者簡介76
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