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长时程增强伴随着锥体神经元树突局部兴奋性的增强。

LTP is accompanied by an enhanced local excitability of pyramidal neuron dendrites.

作者信息

Frick Andreas, Magee Jeffrey, Johnston Daniel

机构信息

Division of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.

出版信息

Nat Neurosci. 2004 Feb;7(2):126-35. doi: 10.1038/nn1178. Epub 2004 Jan 18.

Abstract

The propagation and integration of signals in the dendrites of pyramidal neurons is regulated, in part, by the distribution and biophysical properties of voltage-gated ion channels. It is thus possible that any modification of these channels in a specific part of the dendritic tree might locally alter these signaling processes. Using dendritic and somatic whole-cell recordings, combined with calcium imaging in rat hippocampal slices, we found that the induction of long-term potentiation (LTP) was accompanied by a local increase in dendritic excitability that was dependent on the activation of NMDA receptors. These changes favored the back-propagation of action potentials into this dendritic region with a subsequent boost in the Ca(2+) influx. Dendritic cell-attached patch recordings revealed a hyperpolarized shift in the inactivation curve of transient, A-type K(+) currents that can account for the enhanced excitability. These results suggest an important mechanism associated with LTP for shaping signal processing and controlling dendritic function.

摘要

锥体神经元树突中信号的传播和整合部分受电压门控离子通道的分布和生物物理特性调控。因此,树突树特定部位这些通道的任何改变都可能局部改变这些信号传导过程。利用大鼠海马切片中的树突和体细胞全细胞记录,结合钙成像,我们发现长时程增强(LTP)的诱导伴随着树突兴奋性的局部增加,这依赖于NMDA受体的激活。这些变化有利于动作电位向该树突区域的逆向传播,随后Ca(2+)内流增加。树突细胞贴附式膜片钳记录显示瞬时A型K(+)电流的失活曲线发生超极化偏移,这可以解释兴奋性增强的原因。这些结果提示了一种与LTP相关的重要机制,用于塑造信号处理和控制树突功能。

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