Kashiwagi Y, Nakamura Y, Miyamae Y, Hashimoto R, Takeda M
Department of Neuropsychiatry, Osaka University Medical School, Suita-shi, Japan.
Neurosci Lett. 1998 Aug 7;252(1):5-8. doi: 10.1016/s0304-3940(98)00505-9.
Although chronic aluminum neurotoxicity has been well established, the mechanism of the toxicity has not been elucidated yet. In order to simplify the study of the aluminum neurotoxicity, we employed the pulse exposure of cultured rat cortical neurons to 250 microM aluminum-maltol for 1 h at the early stage (6 h after plating), which resulted in abnormal distribution of neurofilament L (NFL) and fast axonal transported proteins, whereas the axonal transport of tubulin, actin, and clathrin were not impaired. Otherwise, the pulse exposure of neurons at the late stage (4 days after plating) to the same concentration of aluminum-maltol did not affect the cell morphology and the distribution of NFL. The pulse exposure of cultured neurons to aluminum-maltol at the early stage might affect the axonal transport system of NFL and fast axonal transported proteins.
尽管慢性铝神经毒性已得到充分证实,但其毒性机制尚未阐明。为了简化铝神经毒性的研究,我们在早期(接种后6小时)对培养的大鼠皮质神经元进行了1小时的250微摩尔麦芽酚铝脉冲暴露,这导致神经丝L(NFL)和快速轴突运输蛋白分布异常,而微管蛋白、肌动蛋白和网格蛋白的轴突运输未受损害。否则,在后期(接种后4天)将神经元暴露于相同浓度的麦芽酚铝脉冲不会影响细胞形态和NFL的分布。早期对培养神经元进行麦芽酚铝脉冲暴露可能会影响NFL的轴突运输系统和快速轴突运输蛋白。