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The Effects of Physical Fatigue on Central Nervous System
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|摘要:||疲勞是正常的生理反應，日常活動、腦力激盪、或劇烈運動之後，經常會有暫時性的疲勞感。慢性疲勞症候群(chronic fatigue syndrome, CFS)則是指持續6個月以上不知原因的疲勞，且伴隨有記憶力或專注力衰退、喉嚨痛、淋巴結腫大、肌肉僵硬或疼痛、關節痛、頭痛、睡眠不佳、用力後疲勞等四種以上症狀。研究顯示慢性疲勞症候群病患血液中有較高的氧化及亞硝化壓力，一般相信NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells)是調控發炎、氧化及亞硝化壓力途徑之主要上游調控者。而疲勞的相關症狀均與神經系統有關，為了進一步瞭解短時間及長時間運動疲勞對中樞神經細胞的影響及其可能的機制，我們以SD大白鼠為對象，利用自動滾輪強迫動物連續運動1周及8周(每天21小時運動/3小時休息)來誘導疲勞，而後以Morris water maze和負重游泳測試分別來評估其空間記憶能力及體耐力。型態學上，除了分析大腦皮質的厚度外，同時以免疫組織化學染色觀察中樞神經組織中星狀神經膠細胞、NF-κB及nNOS (neuronal NO synthase)-immunoreative細胞的密度。另外，為了進一步瞭解個別神經細胞的樹突型態變化，我們以細胞內染料注射方法來探討皮質脊髓徑神經元及海馬迴CA1 (Cornu Ammonis 1)與CA3錐體細胞的樹突叢，分析樹突棘密度的變化。實驗結果顯示，連續運動1周及8周的大鼠在Morris water maze中的表現顯著下降，顯示如此誘導疲勞的動物之空間記憶力衰退且運動能力變差；連續運動1周後的動物負重游泳能力顯著下降，顯示體耐力下降。從通過前連合處的大腦冠狀切面上量測，體感覺運動皮質的厚度在連續運動8周組顯著下降。然而，這兩組動物大腦皮質第五層錐體細胞的密度並無顯著差異，此外，星狀神經膠細胞及表現nNOS的細胞密度也無顯著差異。長時間連續運動組，表現NF-κB的細胞密度則顯著上升。在神經細胞樹突棘密度上，短時間及長時間連續運動組皮質脊髓徑神經元各部位樹突表面的樹突棘密度顯著下降，海馬迴CA1及CA3錐體細胞也出現相同的變化。綜合上述結果，我們推測短時間或長時間的連續運動會經由改變大腦皮質及海馬迴錐體細胞的樹突型態，來影響動物的負重游泳能力及空間記憶學習能力。|
Fatigue is a normal physiological phenomenon after exercise or daily activity. Fatigue that persists for over six months with four or more of the following symptoms: impaired memory or concentration, sore throat, enlargement of lymph nodes, aching or stiff muscles, multi-joint pain, new headaches, unrefreshing sleep or post-exertional fatigue is regarded as chronic fatigue syndrome (CFS). CFS patients often show high oxidative and nitrosative stress and are believed to link to the activation of its major upstream mechanism, the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) pathway. In this study, we used SD rat as a model and used auto-running wheel (21 hours of running daily) to enforce extended exercise for short (1 week) and long (8 weeks) duration to find out how fatigue affects central neurons. Effects on spatial memory and motor endurance were assessed with Morris water maze and weight-loaded forced swimming test respectively. The effects on cytoarchitecture including cortical thickness and densities of layer V pyramidal neurons, astrocytes, NF-κB and nNOS-expression cells were also evaluated. The dendritic arbors and spines of corticospinal neurons and hippocampal CA1 and CA3 pyramidal neurons were studied following intracellular dye injection. Our results showed 1 or 8 weeks of continuous exercise weakened the animals' performance in Morris water maze and weight-loaded forced swimming test. Cortical thickness at the level of anterior commissure was significant reduced after 8 weeks of continuous exercise. Density of layer V pyramidal neurons as well as those of the GFAP and nNOS-immunoreacitve cells was not altered. Cells expressing NF-κB was however increased after 8 weeks of continuous exercise. Dendritic spines on corticospinal and hippocampal CA1 and CA3 pyramidal neurons of both exercise groups were significantly reduced. In conclusion, our results suggest that extended exercise as short as 1 week could alter the dendritic morphologies of corticospinal as well as hippocampal CA1 and CA3 pyramidal neurons. This might have consequently impaired animals' spatial learning and motor endurance.
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