Light activation, adaptation, and cell survival functions of the Na +/Ca2+ exchanger CalX

Tao Wang, Hong Xu, Johannes Oberwinkler, Yuchun Gu, Roger C. Hardie, Craig Montell

Research output: Contribution to journalArticlepeer-review

Abstract

In sensory neurons, Ca2+ entry is crucial for both activation and subsequent attenuation of signaling. Influx of Ca2+ is counterbalanced by Ca2+ extrusion, and Na+/Ca2+ exchange is the primary mode for rapid Ca2+ removal during and after sensory stimulation. However, the consequences on sensory signaling resulting from mutations in Na+/Ca2+ exchangers have not been described. Here, we report that mutations in the Drosophila Na +/Ca2+ 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 Ca2+ for proper signaling and provide genetic evidence that Ca2+ overload is responsible for a form of retinal degeneration resulting from defects in the TRP channel.

Original languageEnglish (US)
Pages (from-to)367-378
Number of pages12
JournalNeuron
Volume45
Issue number3
DOIs
StatePublished - Feb 3 2005

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Light activation, adaptation, and cell survival functions of the Na +/Ca2+ exchanger CalX'. Together they form a unique fingerprint.

Cite this