Milojkovic Bogdan A, Radojicic Mihailo S, Antic Srdjan D
Department of Neurobiology, Yale University, New Haven, Connecticut 06520-8001, USA.
J Neurosci. 2005 Apr 13;25(15):3940-51. doi: 10.1523/JNEUROSCI.5314-04.2005.
One of the fundamental problems in neurobiology is to understand the cellular mechanism for sustained neuronal activity (neuronal UP states). Prefrontal pyramidal neurons readily switch to a long-lasting depolarized state after suprathreshold stimulation of basal dendrites. Analysis of the dendritic input-output function revealed that basal dendrites operate in a somewhat binary regimen (DOWN or UP) in regard to the amplitude of the glutamate-evoked electrical signal. Although the amplitude of the dendritic potential quickly becomes saturated (dendritic UP state), basal dendrites preserve their ability to code additional increase in glutamatergic input. Namely, after the saturation of the plateau amplitude, an additional increase in excitatory input is interpreted as an increase in plateau duration. Experiments performed in tetrodotoxin indicate that the maintenance of a stable depolarized state does not require inhibitory inputs to "balance" the excitation. In the absence of action potential-dependent (network-driven) GABAergic transmission, pyramidal neurons respond to brief (5 ms) glutamate pulses with stable long-lasting (approximately 500 ms) depolarizations. Voltage-sensitive dye recordings revealed that this somatic plateau depolarization is precisely time-locked with the regenerative dendritic plateau potential. The somatic plateau rises a few milliseconds after the onset of the dendritic transient and collapses with the breakdown of the dendritic plateau depolarization. In our in vitro model, the stable long-lasting somatic depolarization (UP state like) is a direct consequence of the local processing of a strong excitatory glutamatergic input arriving on the basal dendrite. The slow component of the somatic depolarization accurately mirrors the glutamate-evoked dendritic plateau potential (dendritic UP state).
神经生物学的基本问题之一是理解神经元持续活动（神经元兴奋状态）的细胞机制。前额叶锥体神经元在对基底树突进行阈上刺激后很容易转换为持久的去极化状态。对树突输入 - 输出功能的分析表明，就谷氨酸诱发的电信号幅度而言，基底树突以某种二元模式（抑制或兴奋）运作。尽管树突电位的幅度很快达到饱和（树突兴奋状态），但基底树突仍保留对谷氨酸能输入额外增加进行编码的能力。也就是说，在平台幅度饱和后，兴奋性输入的额外增加被解释为平台持续时间的增加。在河豚毒素中进行的实验表明，稳定去极化状态的维持不需要抑制性输入来“平衡”兴奋。在没有动作电位依赖性（网络驱动）GABA能传递的情况下，锥体神经元对短暂（5毫秒）的谷氨酸脉冲会产生稳定的持久（约500毫秒）去极化反应。电压敏感染料记录显示，这种体细胞平台去极化与再生性树突平台电位精确地时间锁定。体细胞平台在树突瞬变开始后几毫秒上升，并随着树突平台去极化的崩溃而消失。在我们的体外模型中，稳定的持久体细胞去极化（类似兴奋状态）是基底树突上强烈兴奋性谷氨酸能输入的局部处理的直接结果。体细胞去极化的慢成分准确地反映了谷氨酸诱发的树突平台电位（树突兴奋状态）。
