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首页> 外文期刊>The European Journal of Neuroscience >Both NKCC1 and anion exchangers contribute to Cl - accumulation in postnatal forebrain neuronal progenitors
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Both NKCC1 and anion exchangers contribute to Cl - accumulation in postnatal forebrain neuronal progenitors

机译：NKCC1和阴离子交换子均促进产后前脑神经元祖细胞的Cl-积累。

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摘要

Neuronal progenitors are continuously generated in the postnatal rodent subventricular zone and migrate along the rostral migratory stream to supply interneurons in the olfactory bulb. Nonsynaptic GABAergic signaling affects the postnatal neurogenesis by depolarizing neuronal progenitors, which depends on an elevated intracellular Cl - concentration. However, the molecular mechanism responsible for Cl - accumulation in these cells still remains elusive. Using confocal Ca 2+ imaging, we found that GABA depolarization-induced Ca 2+ increase was either abolished by bumetanide, a specific inhibitor of the Na +-K +-2Cl - cotransporter, or reduced by partial replacement of extracellular Na + with Li +, in the HEPES buffer but not in the CO 2/ buffer. GABA depolarization-induced Ca 2+ increase in CO 2/ buffer was abolished by a combination of bumetanide with the anion exchanger inhibitor DIDS or with the carbonic anhydrase inhibitor acetozalimide. Using gramicidin-perforated patch-clamp recording, we further confirmed that bumetanide, together with DIDS or acetozalimide, reduced the intracellular chloride concentration in the neuronal progenitors. In addition, with BrdU labeling, we demonstrated that blocking of the Na +-K +-2Cl - cotransporter, but not anion exchangers, reduced the proliferation of neuronal progenitors. Our results indicate that both the Na +-K +-2Cl - cotransporter and anion exchangers contribute to the elevated intracellular chloride responsible for the depolarizing action of GABA in the postnatal forebrain neuronal progenitors. However, the Na +-K +-2Cl - cotransporter displays an additional effect on neuronal progenitor proliferation.
机译：神经元祖细胞在产后啮齿动物的脑室下区域连续产生，并沿着鼻尖迁移流迁移，以在嗅球中提供中间神经元。非突触GABA能信号通过使神经元祖细胞去极化来影响产后神经发生，这取决于细胞内Cl-浓度的升高。然而，负责这些细胞中Cl-积累的分子机制仍然难以捉摸。使用共聚焦Ca 2+成像，我们发现GABA去极化诱导的Ca 2+升高被布美他尼（Na + -K + -2Cl-共转运蛋白的特异性抑制剂）消除，或被Li替代部分细胞外Na +降低了+，在HEPES缓冲区中，但不在CO 2 /缓冲区中。布美他尼与阴离子交换抑制剂DIDS或碳酸酐酶抑制剂乙酰唑胺的组合消除了GABA去极化诱导的CO 2 /缓冲液中Ca 2+的增加。使用青霉菌素穿孔的膜片钳记录，我们进一步证实布美他尼与DIDS或乙酰唑胺一起减少了神经元祖细胞中的细胞内氯化物浓度。此外，使用BrdU标记，我们证明了Na + -K + -2Cl-共转运蛋白的阻滞（而不是阴离子交换剂）的阻滞减少了神经元祖细胞的增殖。我们的结果表明，Na + -K + -2Cl-共转运体和阴离子交换剂均对细胞内氯化物的升高起了作用，从而导致出生后前脑神经元祖细胞中GABA的去极化作用。但是，Na + -K + -2Cl-共转运蛋白对神经元祖细胞增殖显示出附加作用。

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