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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Upregulation of a T-type Ca2+ channel causes a long-lasting modification of neuronal firing mode after status epilepticus.
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Upregulation of a T-type Ca2+ channel causes a long-lasting modification of neuronal firing mode after status epilepticus.

机译：T型Ca2 +通道的上调会导致癫痫持续状态后神经元放电模式的长期改变。

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摘要

A single episode of status epilepticus (SE) causes numerous structural and functional changes in the brain that can lead to the development of a chronic epileptic condition. Most studies of this plasticity have focused on changes in excitatory and inhibitory synaptic properties. However, the intrinsic firing properties that shape the output of the neuron to a given synaptic input may also be persistently affected by SE. Thus, 54% of CA1 pyramidal cells, which normally fire in a regular mode, are persistently converted to a bursting mode after an episode of SE induced by the convulsant pilocarpine. In this model, intrinsic bursts evoked by threshold-straddling depolarizations, and their underlying spike afterdepolarizations (ADPs), were resistant to antagonists of N-, P/Q-, or L-type Ca2+ channels but were readily suppressed by low (30-100 microm) concentrations of Ni2+ known to block T- and R-type Ca2+ channels. The density of T-type Ca2+ currents, but not of other pharmacologically isolated Ca2+ current types, was upregulated in CA1 pyramidal neurons after SE. The augmented T-type currents were sensitive to Ni2+ in the same concentration range that blocked the novel intrinsic bursting in these neurons (IC50 = 27 microm). These data suggest that SE may persistently convert regular firing cells to intrinsic bursters by selectively increasing the density of a Ni2+-sensitive T-type Ca2+ current. This nonsynaptic plasticity considerably amplifies the output of CA1 pyramidal neurons to synaptic inputs and most probably contributes to the development and expression of an epileptic condition after SE.
机译：癫痫持续状态（SE）的单次发作会导致大脑发生许多结构和功能变化，从而导致慢性癫痫病的发展。关于这种可塑性的大多数研究都集中在兴奋性和抑制性突触特性的变化上。但是，使神经元输出到给定突触输入的内在激发特性也可能会受到SE的持续影响。因此，在惊厥性毛果芸香碱诱发的SE发作之后，通常以常规模式激发的54％的CA1锥体细胞被持久地转化为爆发模式。在此模型中，阈跨跨去极化引起的内在爆发及其潜在的去极化后去极化（ADP）对N-，P / Q-或L型Ca2 +通道的拮抗剂具有抗性，但很容易被低（30-已知100微米浓度的Ni2 +会阻断T型和R型Ca2 +通道。 SE后，CA1锥体神经元中T型Ca2 +电流的密度上调，但其他药理分离的Ca2 +电流类型则未上调。增强的T型电流在相同的浓度范围内对Ni2 +敏感，从而阻止了这些神经元中的新的内在爆发（IC50 = 27微米）。这些数据表明，SE可以通过有选择地增加Ni2 +敏感的T型Ca2 +电流的密度来持续地将规则的发射细胞转换为内在的爆发细胞。这种非突触可塑性极大地放大了CA1锥体神经元向突触输入的输出，最有可能有助于SE后癫痫病的发展和表达。

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