目的将在 vivo 在老鼠在长期的 potentiation (LTP ) 和 AMPA 受体子单元上探索暴露的效果到铝(艾尔) 。aluminum-maltolate 建筑群的方法不同剂量[艾尔(mal ) 3 ] 经由尖锐 intracerebroventricular (i.c.v ) 被给老鼠注射和 subchronic intraperitoneal (i.p ) 注射。后面的艾尔暴露,海马趾的 LTP 被地 potentiation 技术从老鼠马头鱼尾的怪兽的 CA1 区域在全部、充实膜的摘录在 vivo 和 AMPAR 子单元蛋白质(GluR1 和 GluR2 ) 的表示记录被西方的污点试金检测。敏锐的艾尔处理生产了的结果在老鼠马头鱼尾的怪兽和在膜的 GluR1 和 GluR2 的剂量依赖者减少的 LTP 的剂量依赖者抑制提取;然而,没有类似的变化在全部的房间摘录被发现,它在马头鱼尾的怪兽从细胞内部的水池建议 AMPA 受体子单元的减少的 trafficking 到 synaptic 地点。LTP 和在膜并且在全部的摘录的 AMPA 受体子单元的表示上的镇压效果在 subchronic 艾尔处理以后被发现的剂量依赖者,在子单元的表示从细胞内部的水池在 AMPA 受体子单元 trafficking 显示减少到 synaptic 地点和另外的减小。结论艾尔(mal ) 在老鼠的 3 显然并且 dose-dependently 压制的 LTP 在 vivo 的海马趾的 CA1 区域,和这抑制可能在 AMPA 受体子单元蛋白质的表示与 trafficking 和减少有关。然而,位于这些观察下面的机制需要推进调查。
Objective To explore the effects of exposure to aluminum (AI) on long-term potentiation (LTP) and AMPA receptor subunits in rats in vivo. Methods Different dosages of aluminum-maltolate complex [Al(mal)3] were given to rats via acute intracerebroventricular (i.c.v.) injection and subchronic intraperitoneal (i.p.) injection. Following AI exposure, the hippocampal LTP were recorded by field potentiation technique in vivo and the expression of AMPAR subunit proteins (GluR1 and GluR2) in both total and membrane-enriched extracts from the CA1 area of rat hippocampus were detected by Western blot assay. Results Acute AI treatment produced dose-dependent suppression of LTP in the rat hippocampus and dose-dependent decreases of GluRz and GluR2 in membrane extracts; however, no similar changes were found in the total cell extracts, which suggests decreased trafficking of AMPA receptor subunits from intracellular pools to synaptic sites in the hippocampus. The dose-dependent suppressive effects on LTP and the expression of AMPA receptor subunits both in the membrane and in total extracts were found after subchronic AI treatment, indicating a decrease in AMPA receptor subunit trafficking from intracellular pools to synaptic sites and an additional reduction in the expression of the subunits. Conclusion Al(mal)3 obviously and dose-dependently suppressed LTP in the rat hippocampal CA1 region in vivo, and this suppression may be related to both trafficking and decreases in the expression of AMPA receptor subunit proteins. However, the mechanisms underlying these observations need further investigation.