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首页> 外文期刊>Neuron >Light activation, adaptation, and cell survival functions of the Na+/Ca2+ exchanger CalX.
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Light activation, adaptation, and cell survival functions of the Na+/Ca2+ exchanger CalX.

机译：Na + / Ca2 +交换剂CalX的光激活，适应和细胞存活功能。

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摘要

In sensory neurons, Ca(2+) entry is crucial for both activation and subsequent attenuation of signaling. Influx of Ca(2+) is counterbalanced by Ca(2+) extrusion, and Na(+)/Ca(2+) exchange is the primary mode for rapid Ca(2+) removal during and after sensory stimulation. However, the consequences on sensory signaling resulting from mutations in Na(+)/Ca(2+) exchangers have not been described. Here, we report that mutations in the Drosophila Na(+)/Ca(2+) exchanger calx have a profound effect on activity-dependent survival of photoreceptor cells. Loss of CalX activity resulted in a transient response to light, a dramatic decrease in signal amplification, and unusually rapid adaptation. Conversely, overexpression of CalX had reciprocal effects and greatly suppressed the retinal degeneration caused by constitutive activity of the TRP channel. These results illustrate the critical role of Ca(2+) for proper signaling and provide genetic evidence that Ca(2+) overload is responsible for a form of retinal degeneration resulting from defects in the TRP channel.
机译：在感觉神经元中，Ca（2+）的进入对于信号的激活和随后的衰减都至关重要。 Ca（2+）的涌入通过Ca（2+）的挤压来抵消，并且Na（+）/ Ca（2+）交换是在感官刺激期间和之后快速去除Ca（2+）的主要方式。但是，尚未描述由Na（+）/ Ca（2+）交换子突变引起的对传感信号的影响。在这里，我们报告果蝇Na（+）/ Ca（2+）交换器calx中的突变对感光细胞的活性依赖性生存产生了深远的影响。 CalX活性的丧失导致对光的瞬态响应，信号放大的急剧下降以及异常迅速的适应。相反，CalX的过表达具有相互影响，并极大地抑制了由TRP通道的组成性活性引起的视网膜变性。这些结果说明了Ca（2+）对于适当的信号转导的关键作用，并提供了Ca（2+）超载是造成TRP通道缺陷导致的视网膜变性形式的遗传证据。

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