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首页> 外文期刊>Journal of Neurophysiology >Indirectly gated Cl(-)-dependent Cl(-) channels sense physiological changes of extracellular chloride in the leech.
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Indirectly gated Cl(-)-dependent Cl(-) channels sense physiological changes of extracellular chloride in the leech.

机译：间接门控Cl（-）依赖Cl（-）通道感应水sense中细胞外氯化物的生理变化。

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The maintenance of ion homeostasis requires adequate ion sensors. In leeches, 34 nephridial nerve cells (NNCs) monitor the Cl(-) concentration of the blood. After a blood meal, the Cl(-) concentration of leech blood triples and is gradually restored to its normal value within 48 h after feeding. As previously shown in voltage-clamp experiments, the Cl(-) sensitivity of the NNCs relies on a persistent depolarizing Cl(-) current that is turned off by an increase of the extracellular Cl(-) concentration. The activation of this Cl(-)-dependent Cl(-) current is independent of voltage and of extra- and intracellular Ca(2+). The transduction mechanism is now characterized on the single-channel level. The NNC's sensitivity to Cl(-) is mediated by a slowly gating Cl(-)-dependent Cl(-) channel with a mean conductance of 50 pS in the cell-attached configuration. Gating of the Cl(-) channel is independent of voltage, and channel activity is independent of extra- and intracellular Ca(2+). Channel activity and the macroscopic current are reversibly blocked by bumetanide. In outside-out patches, changes of the extracellular Cl(-) concentration do not affect channel activity, indicating that channel gating is not via direct interaction of extracellular Cl(-) with the channel. As shown by recordings in the cell-attached configuration, the activity of the channels under the patch is instead governed by the Cl(-) concentration sensed by the rest of the cell. We postulate a membrane-bound Cl(-)-sensing receptor, which-on the increase of the extracellular Cl(-) concentration-closes the Cl(-) channel via a yet unidentified signaling pathway.
机译：维持离子稳态需要足够的离子传感器。在水ches中，有34个肾病神经细胞（NNC）监视血液的Cl（-）浓度。餐后，水le血液中的Cl（-）浓度增加了两倍，并在喂食后48小时内逐渐恢复到正常值。如先前在电压钳实验中所示，NNC的Cl（-）灵敏度依赖于持续的去极化Cl（-）电流，该电流通过增加细胞外Cl（-）浓度而关闭。此依赖于Cl（-）的Cl（-）电流的激活与电压以及细胞外和细胞内Ca（2+）无关。现在在单通道水平上表征转导机制。 NNC对Cl（-）的敏感性是通过缓慢门控依赖于Cl（-）的Cl（-）通道介导的，在细胞附着结构中平均电导为50 pS。 Cl（-）通道的门控与电压无关，并且通道活性与细胞外和细胞内Ca（2+）无关。布美他尼可逆地阻断通道活性和宏观电流。在由外而外的补丁中，细胞外Cl（-）浓度的变化不会影响通道活性，这表明通道门控不是通过细胞外Cl（-）与通道的直接相互作用。如细胞附着配置中的记录所示，贴片下的通道活动由细胞其余部分感测到的Cl（-）浓度决定。我们假设一个膜结合的Cl（-）感应受体，它在细胞外Cl（-）浓度增加时通过一个尚未确定的信号通路关闭Cl（-）通道。

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