臺灣國際科展

長期服用安非他命對小鼠腦部紋狀體內蛋白質表

科展類別
臺灣國際科展
屆次
2004年
科別
醫學與健康科學
學校名稱
國立臺灣師範大學附屬高級中學
指導老師
陳儀莊、謝慧齡
作者
李佩芝
關鍵字
安非他命,腦部,蛋白質
備註
香港第卅七屆聯校科學展覽會正選代表

摘要或動機

安非他命的濫用在台灣是非常嚴重的公眾健康及社會問題。安非他命會導致一連串的行為異常,包括在中腦紋狀體內釋放多巴胺及阻止多巴胺回收來增加使用者的活動力。由於安非他命會對腦細胞造成傷害,本研究的目的為探討低劑量、無立即毒性之安非他命(類似於人類使用習慣)長期施打下,是否會對C57BL6 小鼠大腦紋狀體內的蛋白質表現有影響。因此利用西方點墨法分析施打低劑量安非他命(2 到6 mg/kg) 約一星期之後,C57BL6 小鼠的大腦紋狀體中一些重要蛋白質(包括腺.酸受體A2A-R、第五亞型腺.酸環化.AC5、caspase-8 及PARP) 的表現是否有改變。實驗結果顯示,低劑量安非他命處理對這些蛋白質的表現並沒有明顯的差異。但利用二維電泳法可看到有少許蛋白質,在經過安非他命處理下有顯著的差別,如KIAA0193 homolog 、GOS-28、gammacrystallin A、malate dehydrogenase 和phosphoglycerate mutase isozyme B (PGAM-B)。這些蛋白質中,malate dehydrogenase 和PGAM-B 與代謝和產生ATP 有關,但前者是增加的,而後者減少,推測安非他命會影響神經細胞的能量代謝,因此長期施打安非他命對紋狀體造成的影響值得進一步探討。;The wide spreading use of amphetamine (AMPH) in Taiwan has become a serious public health and social problem. AMPH evokes a series of behavior abnormality including enhanced locomotor behavior by releasing dopamine and inhibiting dopamine-uptake in the striatum. Since AMPH is known to cause brain damage, the purpose of this study is to investigate the expression of several important proteins in the striatum of C57BL6 mice after chronic treatment with low and non-toxic dosages of AMPH (mimicking the common usage pattern of AMPH addict). C57BL6 mice were daily IP-injected with various dosages of AMPH (0 to 6 mg/kg) for one week. Expression levels of A2A adenosine receptor (A2A-R), adenylyl cyclase type V (AC5), caspase-8 and PARP in the striatum were analyzed by Western blotting analysis. Most proteins examined were not affected by this 1-week AMPH treatment. By the aid of two-dimensional gel electrophoresis, expressions of a few striatal proteins (such as KIAA0193 homolog, GOS-28, gammacrystallin A, malate dehydrogenase and phosphoglycerate mutase isozyme B (PGAM-B) in AMPH-treated mice were altered. Note that malate dehydrogenase and PGAM-B are two enzymes involved in energy metabolism and ATP generation. Interestingly, the former was increased and while the latter was decreased in AMPH-treated mice. Collectively AMPH may affect the energy metabolism in neuronal cells. These results suggest that the injury induced by long-term AMPH exposure warrants our further concerns and investigation.


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