Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/52699
標題: 疲勞對公鼠大腦皮質神經細胞形態之影響
The Morhphological Effects of the Cortical Neurons in the Rat after Fatigue
作者: 陳建榮
王慈娟
關鍵字: 基礎研究
fatigue
畜牧獸醫類
疲勞
皮質脊髓徑神經元
前庭脊髓徑神經元
海馬回
樹突
細胞內染料注射
蛋白電泳
免疫組織染色
corticospinal neuron
vestibulospinal neuron
hippocampus
dendriticmorphology
intracellular dye injection
protein electrophoresis
immunohistochemistry
摘要: 生活緊湊及工作壓力常衍生出疲勞,進而導致活動力及肌耐力降低、注意力不集中、記憶力下降。這些症狀可能中樞神經有密切關係。我們的前置實驗顯示, 睡眠干擾造成公鼠負重游泳能力及水迷宮記憶反應變差,皮質及海馬回細胞樹突棘減少,大腦內PSD95 減少,顯示疲勞會改變大腦的神經聯繫。本計畫第一年擬先以睡眠干擾的生理疲勞及注射polyI:C 的免疫疲勞模式來探討行為反應如何變差,同時以細胞內染料注射探討雄性大鼠皮質脊髓徑、海馬回CA1 及CA3、前庭脊髓徑神經細胞的樹突變化;第二年則分析評估PSD 95, synaptophysin, synaptobrevin 及spinophilin 等突觸相關之蛋白與行為變化及樹突變化的連動關係;同時探討去除疲勞的壓力後,形態改變是否能恢復?再以免疫織染色法探討大腦皮質中serotonin transporter 的分佈是否因疲勞而改變?另外也將進行重覆疲勞後,觀察腦區中樹突的變化;第三年則探討目前常用降低運動疲勞的BCAAs 及喧稱能消除疲勞的咖啡因或中草藥碎取物是否能預防或去除疲勞所引起的中樞神經元樹突變化。實驗結果將促進我們瞭解疲勞對負責感覺運動的皮質神經元和前庭脊髓徑神經元以及可能與記憶有關的海馬回神經細胞的影響,除提供未來實驗的依據外,更希望從中找出樹突形態改變與疲勞間的因果關係,提供未來疲勞藥物或產品開發及臨床醫療的參考。
Fatigue, a common phenomenon associated with the working and social stress ofmodern life, results in symptoms including decreasing activities and muscle endurance andimpaired concentration, attention, and memory. Most of these symptoms are closely related tothe functioning of the central nervous system and suggest alteration of cortical functions. Ourpreliminary studies show that sleep disturbance-induced fatigue decreased the physicalstrength and also the spatial memory of rats in a few days. This was associated with areduction of the dendritic spines on corticospinal and hippocampal neurons, and decrease ofthe postsynaptic density-associated protein PSD-95 indicating that fatigue can alter centralneuronal connection. In the first year of this proposal, we will explore whether and howsleep-disturbance fatigue and polyI:C injection-induced immune-fatigue alter the dendriticarbors and dendritic spines of corticospinal, vestibulospinal and hippocampal CA1 and CA3pyramidal neurons of rats, as these neurons are critical to the their sensorimotor function andmemory respectively. In the second year, we will explore whether synapse-related proteins,PSD 95, synaptophysin, synaptobrevin and spinophilin are altered following fatigue? How arethe time courses of these changes correlate with the behavioral changes and morphologicalchanges of these neurons? Are the fatigue-induced central neuronal changes reversible?Whether fatigue alters the distribution of serotonin transporter as serotonin level wassuggested to be altered during fatigue. How does repetitive fatigue exposure alter the dendriticmorphology of these central neurons? In the third year, we will explore whether BCAAs,thought to be capable of relieving exercise-induced fatigue, caffeine-containing supplement,and some of the classical Chinese herb extracts claimed to be useful in relieving fatigue canprevent or restore the neuronal dendritic changes studied. Results obtained will further ourunderstanding on whether and how sleep and immune- fatigue may alter central functioningby changing neuronal dendritic structures, thus the connectivity of central neurons. These willnot only serve scientifically to evaluate the extent of fatigue and may also allow us to exploreor assess fatigue medicine especially on the prevention and on how to enhance the recovery ofcentral neurons from fatigue-induced dendritic regression.
URI: http://hdl.handle.net/11455/52699
其他識別: NSC97-2313-B005-045
文章連結: http://grbsearch.stpi.narl.org.tw/GRB/result.jsp?id=1663005&plan_no=NSC97-2313-B005-045&plan_year=97&projkey=PD9709-0233&target=plan&highStr=*&check=0&pnchDesc=%E7%96%B2%E5%8B%9E%E5%B0%8D%E5%85%AC%E9%BC%A0%E5%A4%A7%E8%85%A6%E7%9A%AE%E8%B3%AA%E7%A5%9E%E7%B6%93%E7%B4%B0%E8%83%9E%E5%BD%A2%E6%85%8B%E4%B9%8B%E5%BD%B1%E9%9F%BF
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