Bernard C, Johnston D
Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.
J Neurophysiol. 2003 Sep;90(3):1807-16. doi: 10.1152/jn.00286.2003.
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 approximately 260 micrometer from the soma, 260 approximately 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.
在海马体CA1锥体神经元中，轴突产生的动作电位以递减的方式反向传播到树突中，在那里它们影响突触整合和突触可塑性。反向传播动作电位（b-APs）的幅度受多种生物学因素控制，包括膜电位（Vm）。我们报告，在任何树突位置（x），当Vm超过阈值电位x时，反向传播会从弱（小幅度b-APs）转变为强（大幅度b-APs）。当Vm > x时，反向传播很强（大多为主动传播）。相反，当Vm < x时，反向传播很弱（大多为被动传播）。x与距胞体的距离（x）呈线性变化。在靠近胞体处，x << 静息膜电位（RMP），膜的强烈超极化是将反向传播从强转换为弱所必需的。在远端树突中，x >> RMP，强烈的去极化是将反向传播从弱转换为强所必需的。在距胞体约260微米处，x约为260，接近RMP，这表明在这个树突区域，反向传播开始从强转换为弱。x取决于Na+和K+通道的可用性或状态。K+通道的部分阻断或磷酸化会降低x，从而增加经历强反向传播的树突部分。Na+通道的部分阻断或失活则有相反的效果。我们得出结论，x是一个捕捉从弱到强反向传播转变起始的参数。其改变可能通过改变大动作电位在树突中反向传播的距离，在生理和病理条件下改变树突功能。
