The site for initiation of action potential discharge over the somatodendritic axis of rat hippocampal CA1 pyramidal neurons
The site for initiation of action potential discharge over the somatodendritic axis of rat hippocampal CA1 pyramidal neurons
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大鼠海马CA1锥体神经元体树突轴动作电位放电起始位点
DOI：
10.1523/jneurosci.11-07-02270.1991
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发表时间：
1991
影响因子：
11.1
通讯作者：
J. Barker
中科院分区：
文献类型：
--
作者：
RW Turner;D. Meyers;TL Richardson;J. Barker
哺乳动物海马的早期电生理研究报告称，锥体细胞的正交去极化在轴突丘和树突树突的一个或多个部位诱发了动作电位放电（假定是Na+依赖）（Cragg和Hamlyn, 1955; Andersen, 1959, 1960； Spencer和Kandel, 1961； Andersen和Lomo， 1966）。虽然在树突水平上已经记录到河豚毒素（TTX）敏感尖峰（Wong et al., 1979; Benardo et al., 1982; Miyakawa and Kato, 1986; Turner et al., 1989），但尚未确定这些电位的起始位置。在这项研究中，我们研究了大鼠海马CA1锥体神经元细胞轴上Na+尖峰放电的起始位置。对体外保存的海马锥体神经元切片进行体内和树突内记录。尖峰放电可由肺泡（反向）刺激引起，也可由东方层（SO）或辐射层（SR）的传入输入刺激引起。在体细胞记录中，倒立和正立的穗状突起振幅最大，沿树突顶端轴逐渐减小；而在细胞体处，穗状突起半宽最短，随离金字塔层的距离增加而增大。正交峰阈值的测量表明，在阈值强度（电压阈值）下，峰以一致的膜电位放电的唯一位置是细胞体区域。最后，在阈值强度下，在锥体层局部应用TTX可以阻断sr诱发的树突内spike，而在阈值以上强度下，需要TTX向树突顶端区域扩散才能阻断spike。这些结果表明，对于阈值强度的刺激，CA1锥体细胞的反斜和正斜尖峰放电在细胞体层区域启动，随后以逆行方式传导到顶端树突。相比之下，sr诱发的正交尖峰放电在树突顶端的起始位置表现出强度依赖的位移，最大位移可达200微米。
Early electrophysiological studies in the mammalian hippocampus reported that orthodromic depolarization of pyramidal cells evoked action potential discharge (presumed Na+ dependent) both at the axon hillock and at one or more sites in the dendritic arborization (Cragg and Hamlyn, 1955; Andersen, 1959, 1960; Spencer and Kandel, 1961; Andersen and Lomo, 1966). Although tetrodotoxin (TTX)-sensitive spikes have been recorded at the dendritic level (Wong et al., 1979; Benardo et al., 1982; Miyakawa and Kato, 1986; Turner et al., 1989), the site for initiation of these potentials has not yet been determined. In this study, we examine the site for initiation of Na+ spike discharge over the cell axis of rat hippocampal CA1 pyramidal neurons. Intrasomatic and intradendritic recordings were obtained from pyramidal neurons of hippocampal slices maintained in vitro. Spike discharge was evoked by alvear (antidromic) stimulation or orthodromically by stimulation of afferent inputs in stratum oriens (SO) or stratum radiatum (SR). Antidromic and orthodromic spikes were greatest in amplitude in somatic recordings and declined over the apical dendritic axis, while spike half-width was shortest at the cell body and increased with distance from stratum pyramidale. Measurements of orthodromic spike threshold revealed that the only location at which spikes discharged at a consistent membrane potential at threshold intensity (voltage threshold) was the cell body region. Finally, at threshold intensity, SR-evoked intradendritic spikes were blocked by local application of TTX in stratum pyramidale, while spike blockade at suprathreshold intensity required the diffusion of TTX into the apical dendritic region. These results indicate that, for threshold intensities of stimulation, antidromic and orthodromic spike discharge in CA1 pyramidal cells is initiated in the region of the cell body layer, subsequently conducting over the apical dendrites in a retrograde fashion. In contrast, SR-evoked orthodromic spike discharge exhibits an intensity-dependent shift in the site of origin up to 200 microns within the apical dendritic arborization.