4.4 Article

Distance-dependent modifiable threshold for action potential back-propagation in hippocampal dendrites

期刊

JOURNAL OF NEUROPHYSIOLOGY
卷 90, 期 3, 页码 1807-1816

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00286.2003

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资金

  1. NIMH NIH HHS [MH-44754, MH-48432] Funding Source: Medline
  2. NINDS NIH HHS [NS-37444] Funding Source: Medline

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In hippocampal CA1 pyramidal neurons, action potentials generated in the axon back-propagate in a decremental fashion into the dendritic tree where they affect synaptic integration and synaptic plasticity. The amplitude of back-propagating action potentials (b-APs) is controlled by various biological factors, including membrane potential ( V m). We report that, at any dendritic location ( x), the transition from weak (small-amplitude b-APs) to strong (large-amplitude b-APs) backpropagation occurs when V-m crosses a threshold potential, theta(x). When V-m > theta(x), back-propagation is strong (mostly active). Conversely, when V-m > theta(x), back-propagation is weak (mostly passive). theta(x) varies linearly with the distance ( x) from the soma. Close to the soma, theta(x) << resting membrane potential (RMP) and a strong hyperpolarization of the membrane is necessary to switch back-propagation from strong to weak. In the distal dendrites, theta(x) >> RMP and a strong depolarization is necessary to switch back-propagation from weak to strong. At similar to 260 mum from the soma, theta(260) approximate to RMP, suggesting that in this dendritic region back-propagation starts to switch from strong to weak. theta(x) depends on the availability or state of Na+ and K+ channels. Partial blockade or phosphorylation of K+ channels decreases theta(x) and thereby increases the portion of the dendritic tree experiencing strong back-propagation. Partial blockade or inactivation of Na+ channels has the opposite effect. We conclude that theta(x) is a parameter that captures the onset of the transition from weak to strong back-propagation. Its modification may alter dendritic function under physiological and pathological conditions by changing how far large action potentials back-propagate in the dendritic tree.

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