Voltage-dependent membrane potential oscillations of rat striatal fast-spiking interneurons
Voltage-dependent membrane potential oscillations of rat striatal fast-spiking interneurons
复制标题
DOI：
10.1113/jphysiol.2003.040857
复制
发表时间：
2003-05-15
影响因子：
5.5
通讯作者：
Calabresi, P
中科院分区：
文献类型：
--
作者：
Bracci, E;Centonze, D;Calabresi, P
我们使用全细胞记录研究阈下膜电位振荡及其与纹状体快速发放中间神经元间歇性放电的关系。在电流注射（100-500 pA，1 s）期间，这些细胞显示出高度可变的峰电位爆发模式（包括1-30个动作电位），其中穿插有膜电位振荡。振荡阈值为-42 +/- 10 mV，与动作电位的阈值一致。振荡频率依赖于电压，范围在20和100 Hz之间。振荡不受钙通道阻滞剂镉和镍和离子型谷氨酸和GABA受体阻滞剂。相反，钠通道阻断剂河豚毒素完全取消的振荡和尖峰爆发。爆发的第一个尖峰似乎是由振荡触发的，因为在亚阈值电压区域中膜电位的上升的时间和速率对于两个事件是相似的。相反，第二个尖峰（以及随后的尖峰）在亚阈值电压范围内显示出快得多的去极化，表明它们是由不同的机制产生的。与这些概念一致，在振荡期间传递的细胞内电流的小脉冲有效地触发了动作电位的爆发，其持续时间大大超过了脉冲。我们的结论是，快速尖峰interneuron振荡产生的内在膜机制，不需要快速的突触传递，这取决于钠电导，但不钙电导，这种振荡是负责触发间歇性尖峰脉冲是典型的这些神经元。
We used whole-cell recordings to investigate subthreshold membrane potential oscillations and their relationship with intermittent firing in striatal fast-spiking interneurons. During current injections (100-500 pA, 1 s), these cells displayed a highly variable pattern of spike bursts (comprising 1-30 action potentials) interspersed with membrane potential oscillations. The oscillation threshold was -42 +/- 10 mV, and coincided with that for action potentials. The oscillation frequency was voltage dependent and ranged between 20 and 100 Hz. Oscillations were unaffected by the calcium channel blockers cadmium and nickel and by blockers of ionotropic glutamate and GABA receptors. Conversely, the sodium channel blocker tetrodotoxin fully abolished the oscillations and the spike bursts. The first spike of a burst appeared to be triggered by an oscillation, since the timing and rate of rise of the membrane potential in the subthreshold voltage region was similar for the two events. Conversely, the second spike (and the subsequent ones) displayed much faster depolarisations in the subthreshold voltage range, indicating that they were generated by a different mechanism. Consistent with these notions, a small pulse of intracellular current delivered during the oscillation was effective in triggering a burst of action potentials that largely outlasted the pulse. We conclude that fast-spiking interneuron oscillations are generated by an intrinsic membrane mechanism that does not require fast synaptic transmission, and which depends on sodium conductance but not calcium conductance, and that such oscillations are responsible for triggering the intermittent spike bursts that are typical of these neurons.