Journal
NATURE NEUROSCIENCE
Volume 8, Issue 1, Pages 43-50Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn1362
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- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R37GM030997] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS047715] Funding Source: NIH RePORTER
- NIGMS NIH HHS [R37 GM030997, GM20997] Funding Source: Medline
- NINDS NIH HHS [R01 NS047715-01A1, R01 NS047715] Funding Source: Medline
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Transformation of mechanical energy into ionic currents is essential for touch, hearing and nociception. Although DEG/ENaC proteins are believed to form sensory mechanotransduction channels, the evidence for this role remains indirect. By recording from C. elegans touch receptor neurons in vivo, we found that external force evokes rapidly activating mechanoreceptor currents (MRCs) carried mostly by Na+ and blocked by amiloride-characteristics consistent with direct mechanical gating of a DEG/ENaC channel. Like mammalian Pacinian corpuscles, these neurons depolarized with both positive and negative changes in external force but not with sustained force. Null mutations in the DEG/ENaC gene mec-4 and in the accessory ion channel subunit genes mec-2 and mec-6 eliminated MRCs. In contrast, the genetic elimination of touch neuron-specific microtubules reduced, but did not abolish, MRCs. Our findings link the application of external force to the activation of a molecularly defined metazoan sensory transduction channel.
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