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題 名 | Chronic Morphine Exposure Enhanced NMDA Receptor-Mediated Cytotoxicity in Primary Cortical Cells=慢性給予嗎啡可增強NMDA對大白鼠大腦混合皮質細胞誘導的細胞毒性 |
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作 者 | 高玉勳; 吳劍男; 謝文雅; 陶寶綠; 楊忠謀; 楊生湳; | 書刊名 | 醫學研究 |
卷 期 | 21:3 2001.06[民90.06] |
頁 次 | 頁159-168 |
分類號 | 418.2132 |
關鍵詞 | 慢性嗎啡處理; 細胞毒性; Chronic morphine exposure; NMDA; Cytotoxicity; |
語 文 | 英文(English) |
中文摘要 | 若母親對嗎啡有成癮習慣,則其有高比例的嬰兒孩出生後有脫癮的現象,且神經系統發育及學習功能也有遲緩的情形。此外,長期給予懷孕母鼠嗎啡,其子代海馬迴N-methy-D-aspartate (NMDA)受器的數目相較於控制組有顯著性差異;且嗎啡組子代海馬迴CA1突處區NMDA受器的最大電流強度顯著高於控制組子代。因此,慢性給予嗎啡可增強子代中樞神經細胞NMDA受器的功能。然而對於慢性給予嗎啡是否增強中樞神經細胞NMDA所誘導的細胞毒性,截至目前為止尚不是很清楚。因此本實驗應用大腦混合皮質細胞來探討慢性給予嗎啡是否會增強中樞神經細胞NMDA所誘導的細胞毒性。結果顯示單獨給予嗎啡(10¯⁴ - 10¯² M)或NMDA (30-1000 μM),可造成細胞毒性呈現劑量依賴性的增加;此外,慢性給予嗎啡亦會增強中樞神經細胞NMDA所誘導的細胞毒性。綜合以上結果,慢性給予嗎啡會加成性增加中樞神經細胞NMDA所誘導的細胞毒性,而一氧化氮於此加成性之細胞毒性中,似乎未扮演一重要角色;然而慢性給予嗎啡可能會改變NMDA受器的功能,例如鈣離子的內流,進而活化導致加成性毒性產生的病理性機制。 |
英文摘要 | Infants of morphine-addicted mothers had a higher incidence of neonatal abstinence syndrome and retardation in neurobiological development. Chronic treatment of morphine in pregnant rats changed the number of NMDA receptors in the hippocampus of their offspring. Our previous study indicated that chronic morphine exposure enhanced NMDA receptor-mediated functions in the central nervous system (CNS) of morphine-addicted rats. However, it remains unclear whether chronic morphine exposure could enhance NMDA induced cytotoxicity in the CNS. In this study, we evaluated whether chronic morphine exposure enhanced NMDA induced cytotoxicity in primary mixed cortical cells of rats. Results indicated that morphine (10¯⁴ - 10¯² M) or NMDA (30-1000 μM) addition concentration-dependently produced cytotoxicity. Furthermore, chronic pretreatment of morphine exposure could potentiate NMDA induced cytotoxicity. In conclusion, the results here demonstrated that cytotoxicity was synergistically induced by NMDA in the presence of chronic morphine exposure. It seemed that nitric oxide did not play an important role for this synergistic cytotoxicity. However, it is likely that chronic morphine exposure modulated NMDA receptor-mediated functions, such as an increase of Ca²⁺ influx, and hence activated pathological mechanisms leading to this synergistic cytotoxicity. |
本系統中英文摘要資訊取自各篇刊載內容。