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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >NKCC1 phosphorylation stimulates neurite growth of injured adult sensory neurons.
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NKCC1 phosphorylation stimulates neurite growth of injured adult sensory neurons.

机译：NKCC1磷酸化刺激受伤的成人感觉神经元的神经突生长。

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摘要

Peripheral nerve section promotes regenerative, elongated neuritic growth of adult sensory neurons. Although the role of chloride homeostasis, through the regulation of ionotropic GABA receptors, in the growth status of immature neurons in the CNS begins to emerge, nothing is known of its role in the regenerative growth of injured adult neurons. To analyze the intracellular Cl- variation after a sciatic nerve section in vivo, gramicidin perforated-patch recordings were used to study muscimol-induced currents in mice dorsal root ganglion neurons isolated from control and axotomized neurons. We show that the reversal potential of muscimol-induced current, E(GABA-A), was shifted toward depolarized potentials in axotomized neurons. This was attributable to Cl- influx because removal of extracellular Cl- prevented this shift. Application of bumetanide, an inhibitor of NKCC1 cotransporter and E(GABA-A) recordings in sensory neurons from NKCC1-/- mice, identified NKCC1 as being responsible for the increase inintracellular Cl- in axotomized neurons. In addition, we demonstrate with a phospho-NKCC1 antibody that nerve injury induces an increase in the phosphorylated form of NKCC1 in dorsal root ganglia that could account for intracellular Cl- accumulation. Time-lapse recordings of the neuritic growth of axotomized neurons show a faster growth velocity compared with control. Bumetanide, the intrathecal injection of NKCC1 small interfering RNA, and the use of NKCC1-/- mice demonstrated that NKCC1 is involved in determining the velocity of elongated growth of axotomized neurons. Our results clearly show that NKCC1-induced increase in intracellular chloride concentration is a major event accompanying peripheral nerve regeneration.
机译：周围神经节促进成年感觉神经元的再生，伸长的神经生长。尽管氯化物的稳态作用通过调节离子型GABA受体在中枢神经系统中不成熟神经元的生长状态中开始出现，但对其在受伤的成年神经元的再生生长中的作用尚无定论。为了分析体内坐骨神经切片后的细胞内Cl-变化，使用了短杆菌肽穿孔膜片记录研究了由麝香酚诱导的小鼠背根神经节神经元电流，该电流是从对照神经元和轴突化神经元中分离出来的。我们表明，muscimol诱导的电流，E（GABA-A）的逆转势向着轴突化神经元的去极化势。这归因于Cl-内流，因为去除细胞外Cl-阻止了这种转变。布美他尼是NKCC1共转运蛋白和E（GABA-A）抑制剂在来自NKCC1-/-小鼠的感觉神经元中的应用的应用，确定NKCC1引起了被切除神经元的细胞内Cl-的增加。此外，我们用磷酸化-NKCC1抗体证明神经损伤诱导背根神经节中磷酸化形式的NKCC1的增加，这可能是细胞内Cl-积累的原因。与对照相比，轴突切除的神经元的神经生长的延时记录显示出更快的生长速度。布美他尼，鞘内注射NKCC1小干扰RNA以及使用NKCC1-/-小鼠证明NKCC1参与确定轴突切除神经元的延长生长速度。我们的结果清楚地表明，NKCC1诱导的细胞内氯化物浓度增加是伴随周围神经再生的主要事件。

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