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目的:探讨荷包牡丹碱(BiC)对海马CA2区的神经毒性作用以及电压依赖性钙通道(VDCC)对神经毒性作用的影响。方法:BiC 6μmol·L~(-1)刺激培养的大鼠海马组织72 h,同时用N,L以及P/Q型钙通道拮抗剂分别阻断相应的钙通道,测定神经细胞摄取的碘化丙啶(PI)。结果:BiC刺激6 h后,神经细胞的PI摄取首先出现在CA2区。随着BiC刺激时间的延长,摄取PI的神经细胞的分布范围由CA2区扩散到其他区域。P/Q型VDCC拮抗剂抑制神经细胞的PI摄取,然而N和L型VDCC的拮抗剂无明显抑制效果。结论:在大鼠海马的组织培养中CA2区的神经细胞对BiC的刺激最易受损。CA2区神经细胞的损伤过程中P/Q型VDCC起重要作用。
Objective: To investigate the neurotoxic effect of bicuculline (BIC) on hippocampal CA2 region and the effect of voltage-dependent calcium channel (VDCC) on neurotoxicity. Methods: The hippocampus of cultured rat hippocampus was stimulated with BiC 6 μmol·L -1 for 72 h, and the corresponding calcium channels were blocked by N, L and P / Q type calcium channel blockers, respectively. The iodide uptake by nerve cells Propidium (PI). Results: After 6 h of BiC stimulation, PI uptake in nerve cells first appeared in CA2 area. With the prolongation of BiC stimulation, the distribution of PI-uptake neurons spread from CA2 region to other regions. P / Q type VDCC antagonists inhibited PI uptake in nerve cells, whereas antagonists of N and L type VDCC showed no significant inhibitory effect. CONCLUSION: Neurons in CA2 area are most vulnerable to BiC stimulation in the tissue culture of rat hippocampus. P / Q type VDCC plays an important role in the damage of CA2 nerve cells.