Schwindt P, Crill W
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98195-7290, USA.
J Neurophysiol. 1999 Mar;81(3):1341-54. doi: 10.1152/jn.1999.81.3.1341.
Apical dendrites of layer 5 pyramidal cells in a slice preparation of rat sensorimotor cortex were depolarized focally by long-lasting glutamate iontophoresis while recording intracellularly from their soma. In most cells the firing pattern evoked by the smallest dendritic depolarization that evoked spikes consisted of repetitive bursts of action potentials. During larger dendritic depolarizations initial burst firing was followed by regular spiking. As dendritic depolarization was increased further the duration (but not the firing rate) of the regular spiking increased, and the duration of burst firing decreased. Depolarization of the soma in most of the same cells evoked only regular spiking. When the dendrite was depolarized to a critical level below spike threshold, intrasomatic current pulses or excitatory postsynaptic potentials also triggered bursts instead of single spikes. The bursts were driven by a delayed depolarization (DD) that was triggered in an all-or-none manner along with the first Na+ spike of the burst. Somatic voltage-clamp experiments indicated that the action current underlying the DD was generated in the dendrite and was Ca2+ dependent. Thus the burst firing was caused by a Na+ spike-linked dendritic Ca2+ spike, a mechanism that was available only when the dendrite was adequately depolarized. Larger dendritic depolarization that evoked late, constant-frequency regular spiking also evoked a long-lasting, Ca2+-dependent action potential (a "plateau"). The duration of the plateau but not its amplitude was increased by stronger dendritic depolarization. Burst-generating dendritic Ca2+ spikes could not be elicited during this plateau. Thus plateau initiation was responsible for the termination of burst firing and the generation of the constant-frequency regular spiking. We conclude that somatic and dendritic depolarization can elicit quite different firing patterns in the same pyramidal neuron. The burst and regular spiking observed during dendritic depolarization are caused by two types of Ca2+-dependent dendritic action potentials. We discuss some functional implications of these observations.
在大鼠感觉运动皮层的脑片制备中，对第5层锥体神经元的顶端树突进行长效谷氨酸离子电泳局部去极化，同时从其胞体进行细胞内记录。在大多数细胞中，由引发动作电位的最小树突去极化所诱发的放电模式由重复的动作电位爆发组成。在较大的树突去极化过程中，最初的爆发式放电之后是规则发放。随着树突去极化进一步增加，规则发放的持续时间（而非发放频率）增加，爆发式放电的持续时间减少。在大多数相同细胞中，胞体去极化仅诱发规则发放。当树突去极化到低于动作电位阈值的临界水平时，胞内电流脉冲或兴奋性突触后电位也会触发爆发式放电而非单个动作电位。这些爆发式放电由一个延迟去极化（DD）驱动，该延迟去极化与爆发式放电的第一个Na⁺动作电位一起以全或无的方式触发。胞体电压钳实验表明，DD背后的动作电流在树突中产生且依赖于Ca²⁺。因此，爆发式放电是由一个与Na⁺动作电位相关的树突Ca²⁺动作电位引起的，这种机制仅在树突充分去极化时才会出现。诱发晚期、恒定频率规则发放的较大树突去极化也会诱发一个持久的、依赖于Ca²⁺的动作电位（一个“平台电位”）。更强的树突去极化会增加平台电位的持续时间而非其幅度。在这个平台电位期间无法诱发产生爆发式放电的树突Ca²⁺动作电位。因此，平台电位的起始导致了爆发式放电的终止和恒定频率规则发放的产生。我们得出结论，胞体和树突去极化在同一个锥体神经元中可以引发截然不同的放电模式。在树突去极化过程中观察到的爆发式放电和规则发放是由两种依赖于Ca²⁺的树突动作电位引起的。我们讨论了这些观察结果的一些功能意义。
