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Imaging of calcium variations in living dendritic spines of cultured rat hippocampal neurons.

机译:成像的大鼠海马神经元的活树突棘中钙变化的成像。

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摘要

1. Cultured rat hippocampal neurons were loaded with the Ca2+ indicator fura-2 through micropipettes and visualized with an inverted microscope equipped with a high power objective and a cooled CCD camera. The responses of dendritic spines and their parent dendrites to stimuli which evoke a rise of [Ca2+]i were monitored. 2. NMDA caused a rapid and transient rise in [Ca2+]i, which was more evident in the spine than in the parent dendrite. The recovery in both compartments had the same time course, and was dependent on normal [Na+]o. 3. Application of alpha-latrotoxin, which causes release of neurotransmitters from terminals, produced a rise of [Ca2+]i in the dendritic spines, more than in their parent dendrites. Prolonged exposure to the drug eliminated the spine/dendrite disparity. 4. The presence of voltage-gated calcium channels in dendritic spines is indicated by the enhanced calcium rise in spines rather than dendrites of cells depolarized by either intracellular current injection or by raising [K+]o. This rise was attenuated by nifedipine or verapamil, both L-type channel blockers. 5. It is suggested that the dendritic spine constitutes an independent calcium compartment that is closely linked to the parent dendrite.
机译:1.通过微量移液管向培养的大鼠海马神经元加载Ca2 +指示剂fura-2,并用配有高倍物镜和冷却CCD相机的倒置显微镜可视化。监测树突棘及其亲本树突对引起[Ca2 +] i升高的刺激的反应。 2. NMDA导致[Ca2 +] i迅速而短暂地上升,这在脊柱中比在母树突中更为明显。两个隔室中的恢复具有相同的时间过程,并且取决于正常的[Na +] o。 3.导致神经递质从末端释放的α-拉托毒素的应用导致树突棘中[Ca2 +] i的升高,而不是其母体树突中的升高。长时间接触药物消除了脊柱/树突差异。 4.树突棘中钙离子门控钙通道的存在是通过刺中钙升高而不是通过细胞内电流注入或通过升高[K +] o去极化的细胞的树突来表明的。硝苯地平或维拉帕米(均为L型通道阻滞剂)减弱了这种上升。 5.建议树突状脊柱构成一个独立的钙隔室,该钙隔室与母体树突紧密相连。

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