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Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030
Submitted 24 March 2003; accepted in final form 6 May 2003
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 (Vm). We report that, at any dendritic location (x), the transition from weak (small-amplitude b-APs) to strong (large-amplitude b-APs) back-propagation occurs when Vm crosses a threshold potential,
x. When Vm >
x, back-propagation is strong (mostly active). Conversely, when Vm <
x, back-propagation is weak (mostly passive).
x varies linearly with the distance (x) from the soma. Close to the soma,
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,
x >> RMP and a strong depolarization is necessary to switch back-propagation from weak to strong. At
260 µm from the soma,
260
RMP, suggesting that in this dendritic region back-propagation starts to switch from strong to weak.
x depends on the availability or state of Na+ and K+ channels. Partial blockade or phosphorylation of K+ channels decreases
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
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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