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首页> 外文期刊>Neuron >Recordings from single neocortical nerve terminals reveal a nonselective cation channel activated by decreases in extracellular calcium.
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Recordings from single neocortical nerve terminals reveal a nonselective cation channel activated by decreases in extracellular calcium.

机译：来自单个新皮层神经末梢的记录显示非选择性阳离子通道被细胞外钙减少激活。

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摘要

Synaptic activity causes reductions in cleft [Ca(2+)] that may impact subsequent synaptic efficacy. Using modified patch-clamp techniques to record from single neocortical nerve terminals, we report that physiologically relevant reductions of extracellular [Ca(2+)] ([Ca(2+)](o)) activate voltage-dependent outward currents. These outward currents are carried by a novel nonselective cation (NSC) channel that is indirectly inhibited by various extracellular agents (rank order potency, Gd(3+) > spermidine > Ca(2+) > Mg(2+), typical for [Ca(2+)](o) receptors). The identification of a Ca(2+) sensor-NSC channel pathway establishes the existence of a mechanism by which presynaptic terminals can detect and respond to reductions in cleft [Ca(2+)]. Activation of NSC channels by falls in [Ca(2+)](o) would be expected during periods of high activity in the neocortex and may modulate the excitability of the presynaptic terminal.
机译：突触活动导致裂隙[Ca（2+）]减少，可能会影响随后的突触功效。使用改进的膜片钳技术从单个新皮质神经末梢记录，我们报告说，生理相关的细胞外[Ca（2+）]（[Ca（2 +）]（o））减少激活电压依赖性向外电流。这些外向电流由一个新颖的非选择性阳离子（NSC）通道携带，该通道被各种细胞外剂间接抑制（等级效力，Gd（3+）>亚精胺> Ca（2+）> Mg（2+），通常用于[ Ca（2 +）]（o）受体）。 Ca（2+）传感器-NSC通道通路的鉴定建立了一种机制的存在，通过该机制突触前末端可以检测并响应裂痕[Ca（2+）]的减少。 NSC通道的激活由[Ca（2 +）]（o）的下降而被预期在新皮层的高活性期间可能会调节突触前末端的兴奋性。

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