| Literature DB >> 25456135 |
David A Gorczyca1, Susan Younger2, Shan Meltzer1, Sung Eun Kim2, Li Cheng2, Wei Song2, Hye Young Lee2, Lily Yeh Jan2, Yuh Nung Jan3.
Abstract
A major gap in our understanding of sensation is how a single sensory neuron can differentially respond to a multitude of different stimuli (polymodality), such as propio- or nocisensation. The prevailing hypothesis is that different stimuli are transduced through ion channels with diverse properties and subunit composition. In a screen for ion channel genes expressed in polymodal nociceptive neurons, we identified Ppk26, a member of the trimeric degenerin/epithelial sodium channel (DEG/ENaC) family, as being necessary for proper locomotion behavior in Drosophila larvae in a mutually dependent fashion with coexpressed Ppk1, another member of the same family. Mutants lacking Ppk1 and Ppk26 were defective in mechanical, but not thermal, nociception behavior. Mutants of Piezo, a channel involved in mechanical nociception in the same neurons, did not show a defect in locomotion, suggesting distinct molecular machinery for mediating locomotor feedback and mechanical nociception.Entities:
Mesh:
Substances:
Year: 2014 PMID: 25456135 PMCID: PMC4254518 DOI: 10.1016/j.celrep.2014.10.034
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423