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摘要


麩胺酸(L-Glutamic Acid)是哺乳類中樞神經系統最主要的興奮性傅遞物(Excitatory Neurotransmitter)。但遇量的麩胺酸所引起的過度興奮卻是神經元(Neuron)受到損傷的一大主因,在本論文中,我們發现牛磺酸(Taurine)對於胺酸所引起的神經元損傷具有保護的作用,低濃度(50μM)的麩胺酸就已足狗造成體外培養的神經元(Cultured neuron)嚴重的損傷,在同樣倏件下,如果我们加入25mM的牛磺酸,我們就不能看出麩胺酸對體外培養的神經元有任何的損傷作用。我們進一步證明牛磺酸保護神經元的功能,在於它能阻断或减少因麩胺酸刺激所引起神經元細胞内钙雕子濃度的提高,而不是由於牛磺酸能挫制渗透壓力所造成經胞體積的變化。

並列摘要


Primary cultured neurons are significantly damaged by brief exposure to 0.25mM glutamate (Glu). The neuronal damage, as indicated by cell lysis, was not distinguishable until at least 6 to 8 hour after Glu exposure. Inclusion of taurine at 25mM in the extracellular medium reduced Glu-induced neuronal injury. The neuroprotective effect of taurine was not affected by the presence of taurine transport inhibitors, e.g. guanidinoethyl sulfonate (GES) and β-alanine, indicating that intracellular uptake of taurine is not necessary for the neuroprotection by taurine. The presence of 25mM taurine in the medium did not cause a significant change of total intracellular taurine level during Glutreatment. It also had little effect on Glu-induced cell swelling as indicated by [(superscript 3)H]taurine efflux. However, taurine exhibited a remarkable effect on Glu-induced elevation of intracellular calcium level [Ca(surperscript 2+)](subscript i). Therefore, we conclude that the neuroprotection of taurine against Glu-induced neurotoxicity observed in cultured neurons is primarily a result of reducing the level of [Ca(superscript 2+)](subscript i), rather than serving as an osmoregulator.

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