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大鼠腰脊髓中钾氯协同转运蛋白 2 的发育上调。

Developmental up-regulation of the potassium-chloride cotransporter type 2 in the rat lumbar spinal cord.

机构信息

Laboratoire Plasticité et Physio-Pathologie de la Motricité (UMR6196), Centre National de la Recherche Scientifique (CNRS), Aix-Marseille Université, CNRS, 31 Chemin Joseph Aiguier, F-13402 Marseille Cx 20, France.

出版信息

Neuroscience. 2009 Dec 1;164(2):809-21. doi: 10.1016/j.neuroscience.2009.08.035. Epub 2009 Aug 20.

DOI:10.1016/j.neuroscience.2009.08.035
PMID:19699273
Abstract

The classical GABA/glycine hyperpolarizing inhibition is not observed in the immature spinal cord. GABA(A) and glycine receptors are anions channels and the efficacy of inhibitory transmission in the spinal cord is largely determined by the gradient between intracellular and extracellular chloride concentrations. The concentration of intracellular chloride in neurons is mainly regulated by two cation-chloride cotransporters, the potassium-chloride cotransporter 2 (KCC2) and the sodium-potassium-chloride co-transporter 1 (NKCC1). In this study, we measured the reversal potential of IPSPs (E(IPSP)) of lumbar motoneurons during the first postnatal week and we investigated the expression of KCC2 and NKCC1 in the ventral horn of the spinal cord from the embryonic day 17 to the postnatal day 20 in the rat. Our results suggest that the negative shift of E(IPSP) from above to below the resting membrane potential occurs during the first postnatal week when the expression of KCC2 increases significantly and the expression of NKCC1 decreases. KCC2 immunolabeling surrounded motoneurons, presumably in the plasma membrane and NKCC1 immunolabeling appeared outside this KCC2-labeled fine strip. Taken together, the present results indicate that maturation of chloride homeostasis is not completed at birth in the rat and that the upregulation of KCC2 plays a key role in the shift from depolarizing to hyperpolarizing IPSPs.

摘要

经典的 GABA/甘氨酸超极化抑制作用在未成熟脊髓中观察不到。GABA(A)和甘氨酸受体是阴离子通道,脊髓中抑制性传递的效率在很大程度上取决于细胞内和细胞外氯离子浓度梯度。神经元细胞内氯离子的浓度主要由两种阳离子-氯离子共转运蛋白调节,即钾-氯离子共转运蛋白 2(KCC2)和钠-钾-氯离子共转运蛋白 1(NKCC1)。在这项研究中,我们测量了出生后第一周腰椎运动神经元的 IPSP 反转电位(E(IPSP)),并研究了 KCC2 和 NKCC1 在大鼠胚胎第 17 天到出生后第 20 天脊髓腹角的表达。我们的结果表明,当 KCC2 表达显著增加而 NKCC1 表达减少时,E(IPSP)从膜电位以上向以下的负移发生在出生后第一周。KCC2 免疫标记物环绕运动神经元,可能位于质膜中,而 NKCC1 免疫标记物出现在这个 KCC2 标记的细条之外。综上所述,这些结果表明,在大鼠中,氯离子稳态的成熟在出生时并未完成,并且 KCC2 的上调在从去极化 IPSP 向超极化 IPSP 的转变中起着关键作用。

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