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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Kinetic properties of Cl uptake mediated by Na+-dependent K+-2Cl cotransport in immature rat neocortical neurons.
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Kinetic properties of Cl uptake mediated by Na+-dependent K+-2Cl cotransport in immature rat neocortical neurons.

机译：Na +依赖性K + -2Cl共转运在未成熟大鼠新皮层神经元中介导的Cl吸收的动力学特性。

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摘要

GABA, the main inhibitory neurotransmitter in the adult nervous system, evokes depolarizing membrane responses in immature neurons, which are crucial for the generation of early network activity. Although it is well accepted that depolarizing GABA actions are caused by an elevated intracellular Cl- concentration ([Cl-]i), the mechanisms of Cl- accumulation in immature neurons are still a matter of debate. Using patch-clamp, microfluorimetric, immunohistochemical, and molecular biological approaches, we studied the mechanism of Cl- uptake in Cajal-Retzius (CR) cells of immature [postnatal day 0 (P0) to P3] rat neocortex. Gramicidin-perforated patch-clamp and 6-methoxy-N-ethylquinolinium-microfluorimetric measurements revealed a steady-state [Cl-]i of approximately 30 mM that was reduced to values close to passive distribution by bumetanide or Na+-free solutions, suggesting a participation of Na+-K+-2Cl- cotransport isoform 1 (NKCC1) in maintaining elevated [Cl-]i. Expression of NKCC1 was found in CR cells on the mRNA and protein levels. To determine the contribution of NKCC1 to [Cl-]i homeostasis in detail, Cl- uptake rates were analyzed after artificial [Cl-]i depletion. Active Cl- uptake was relatively slow (47.2 +/- 5.0 microM/s) and was abolished by bumetanide or Na+-free solution. Accordingly, whole-cell patch-clamp recordings revealed a low Cl- conductance in CR cells. The low capacity of NKCC1-mediated Cl- uptake was sufficient to maintain excitatory GABAergic membrane responses, however, only at low stimulation frequencies. In summary, our results demonstrate that NKCC1 is abundant in CR cells of immature rat neocortex and that the slow Cl- uptake mediated by this transporter is sufficient to maintain high [Cl-]i required to render GABA responses excitatory.
机译：GABA是成人神经系统中的主要抑制性神经递质，可引起未成熟神经元的去极化膜反应，这对于早期网络活动的产生至关重要。尽管公认的是，去极化GABA作用是由细胞内Cl-浓度（[Cl-] i）升高引起的，但未成熟神经元中Cl-积累的机制仍是一个有争议的问题。使用膜片钳，微荧光，免疫组织化学和分子生物学方法，我们研究了未成熟[出生后第0天（P0）至P3]大鼠新皮层的Cajal-Retzius（CR）细胞吸收Cl的机制。葛米素穿孔的膜片钳和6-甲氧基-N-乙基喹啉鎓的微荧光测定表明，约30 mM的稳态[Cl-] i可通过布美他尼或无Na +的溶液降低至接近于被动分布的值，表明Na + -K + -2Cl-共转运同工型1（NKCC1）参与维持升高的[Cl-] i。 NKCC1在CR细胞中的mRNA和蛋白质水平表达。为了详细确定NKCC1对[Cl-] i体内稳态的贡献，我们在人为[Cl-] i耗尽后分析了Cl-的吸收率。活性Cl吸收相对较慢（47.2 +/- 5.0 microM / s），被布美他尼或无Na +的溶液废除了。因此，全细胞膜片钳记录显示出CR细胞中低的Cl电导。 NKCC1介导的Cl摄取的低容量足以维持兴奋性GABA能膜反应，但是，仅在低刺激频率下才如此。总而言之，我们的结果表明，NKCC1在未成熟大鼠新皮层的CR细胞中丰富，并且由该转运蛋白介导的缓慢的Cl吸收足以维持使GABA反应具有兴奋性所需的高[Cl-] i。

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