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Dendritic signals from rat hippocampal CA1 pyramidal neurons during coincident pre- and post-synaptic activity: a combined voltage- and calcium-imaging study

机译:大鼠海马CA1锥体神经元在突触前后活动同时发生的树突状信号:电压和钙成像联合研究

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摘要

The non-linear and spatially inhomogeneous interactions of dendritic membrane potential signals that represent the first step in the induction of activity-dependent long-term synaptic plasticity are not fully understood, particularly in dendritic regions which are beyond the reach of electrode measurements. We combined voltage-sensitive-dye recordings and Ca2+ imaging of hippocampal CA1 pyramidal neurons to study large regions of the dendritic arbor, including branches of small diameter (distal apical and oblique dendrites). Dendritic membrane potential transients were monitored at high spatial resolution and correlated with supra-linear [Ca2+]i changes during one cycle of a repetitive patterned stimulation protocol that typically results in the induction of long-term potentiation (LTP). While the increase in the peak membrane depolarization during coincident pre- and post-synaptic activity was required for the induction of supra-linear [Ca2+]i signals shown to be necessary for LTP, the change in the baseline-to-peak amplitude of the backpropagating dendritic action potential (bAP) was not critical in this process. At different dendritic locations, the baseline-to-peak amplitude of the bAP could be either increased, decreased or unaltered at sites where EPSP–AP pairing evoked supra-linear summation of [Ca2+]i transients. We suggest that modulations in the bAP baseline-to-peak amplitude by local EPSPs act as a mechanism that brings the membrane potential into the optimal range for Ca2+ influx through NMDA receptors (0 to −15 mV); this may require either boosting or the reduction of the bAP, depending on the initial size of both signals.
机译:树突状膜电位信号的非线性和空间不均匀相互作用代表了依赖于活性的长期突触可塑性诱导的第一步,这一点还没有被完全理解,特别是在电极测量无法达到的树突状区域中。我们将电压敏感染料记录和海马CA1锥体神经元的Ca 2 + 成像相结合,以研究大面积的树突状乔木,包括小直径的分支(远端的顶端和倾斜的树枝状)。在高空间分辨率下监测树突状膜电位瞬变,并与重复模式刺激方案的一个周期内超线性[Ca 2 + ] i变化相关,该变化通常导致诱导长期增强(LTP)。诱导超线性[Ca 2 + ] i信号需要突触前和突触后同时活动期间峰值膜去极化的增加,这对于LTP来说是必需的,反向传播树突动作电位(bAP)的基线到峰值幅度在此过程中并不重要。在不同树突位置,在EPSP–AP配对引起[Ca 2 + ] i瞬态超线性求和的位点,bAP的基线至峰幅度可能会增加,减少或保持不变。我们认为,局部EPSP对bAP基线至峰幅度的调节可作为一种机制,使膜电位处于通过NMDA受体(0至-15 mV)Ca 2 + 流入的最佳范围);这可能需要提高或降低bAP,具体取决于两个信号的初始大小。

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