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首页> 外文期刊>The European Journal of Neuroscience >Contribution of the potassium-chloride co-transporter KCC2 to the modulation of lumbar spinal networks in mice.
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Contribution of the potassium-chloride co-transporter KCC2 to the modulation of lumbar spinal networks in mice.

机译：氯化钾共转运蛋白KCC2对小鼠腰椎网络调节的贡献。

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Spontaneous activity is observed in most developing neuronal circuits, such as the retina, hippocampus, brainstem and spinal cord. In the spinal cord, spontaneous activity is important for generating embryonic movements critical for the proper development of motor axons, muscles and synaptic connections. A spontaneous bursting activity can be recorded in vitro from ventral roots during perinatal development. The depolarizing action of the inhibitory amino acids gamma-aminobutyric acid and glycine is widely proposed to contribute to spontaneous activity in several immature systems. During development, the intracellular chloride concentration decreases, leading to a shift of equilibrium potential for Cl(-) ions towards more negative values, and thereby to a change in glycine- and gamma-aminobutyric acid-evoked potentials from depolarization/excitation to hyperpolarization/inhibition. The up-regulation of the outward-directed Cl(-) pump, the neuron-specific potassium-chloride co-transporter type 2 KCC2, has been shown to underlie this shift. Here, we investigated whether spontaneous and locomotor-like activities are altered in genetically modified mice that express only 8-20% of KCC2, compared with wild-type animals. We show that a reduced amount of KCC2 leads to a depolarized equilibrium potential for Cl(-) ions in lumbar motoneurons, an increased spontaneous activity and a faster locomotor-like activity. However, the left-right and flexor-extensor alternating pattern observed during fictive locomotion was not affected. We conclude that neuronal networks within the spinal cord are more excitable in KCC2 mutant mice, which suggests that KCC2 strongly modulates the excitability of spinal cord networks.
机译：在大多数发育中的神经元回路（如视网膜，海马，脑干和脊髓）中观察到自发活动。在脊髓中，自发活动对于产生对运动轴突，肌肉和突触连接正常发育至关重要的胚胎运动很重要。在围产期发育期间，可以从腹侧根部记录自发的爆发活动。抑制氨基酸γ-氨基丁酸和甘氨酸的去极化作用被广泛提出，以促进几种不成熟系统中的自发活性。在发育过程中，细胞内氯离子浓度降低，导致Cl（-）离子的平衡电势向更负的值移动，从而导致甘氨酸和γ-氨基丁酸引起的电势从去极化/激发到超极化/抑制。已经显示，向外移动的Cl（-）泵（神经元特异性氯化钾共转运蛋白2型KCC2）的上调是这种转变的基础。在这里，我们调查了与野生型动物相比，在仅表达8-20％的KCC2的转基因小鼠中，自发性和运动性活动是否发生了改变。我们显示，减少量的KCC2会导致腰部运动神经元中Cl（-）离子的去极化平衡电位，增加的自发活动和更快的类似运动的活动。但是，虚拟运动期间观察到的左右和屈伸交替模式不受影响。我们得出的结论是，在KCC2突变小鼠中，脊髓内的神经元网络更容易被兴奋，这表明KCC2强烈调节了脊髓网络的兴奋性。

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