Abstract
Acoustic overexposure, such as listening to loud music too often, results in noise-induced hearing loss. The pathologies of this prevalent sensory disorder begin within the ear at synapses of the primary auditory receptors, their postsynaptic partners and their supporting cells. The extent of noise-induced damage, however, is determined by overstimulation of primary auditory receptors, upstream of where the pathologies manifest. A systematic characterization of the electrophysiological function of the upstream primary auditory receptors is warranted to understand how noise exposure impacts on downstream targets, where the pathologies of hearing loss begin. Here, we used the experimentally-accessible locust ear (male, Schistocerca gregaria) to characterize a decrease in the auditory receptor’s ability to respond to sound after noise exposure. Surprisingly, after noise exposure, the electrophysiological properties of the auditory receptors remain unchanged, despite a decrease in the ability to transduce sound. This auditory deficit stems from changes in a specialized receptor lymph that bathes the auditory receptors, revealing striking parallels with the mammalian auditory system.
| Original language | English |
|---|---|
| Pages (from-to) | 3130-3140 |
| Number of pages | 11 |
| Journal | Journal of Neuroscience |
| Volume | 40 |
| Issue number | 15 |
| DOIs | |
| Publication status | Published - Apr 8 2020 |
Bibliographical note
Funding Information:This work was supported by the Royal Society and the Leverhulme Trust, by the Department of Neuroscience, Psychology, and Behavior Within the University of Leicester, and the Wellcome Trust Institutional Strategic Support Fund to B.W.; by a Royal Society Enhancement Award to G.F.; by the European Research Council under the European Union’s Seventh Framework Program (FP/2007-2013)/ERC Grant 615030 to E.K. and J.F.C.W.; and by Discovery Grant RGPIN/03712 from the Natural Sciences and Engineering Research Council of Canada to A.S.F. We thank Neil Rimmer and Jake Cranston for locust husbandry; Ben Cooper and Brendan O’Connor for help with statistical analysis and making sure the locust treatment remained blinded to the experimenter; and Nathan Suray for performing preliminary experiments for in vivo hook electrode recordings. Correspondence should be addressed to Ben Warren at bw120@le.ac.uk. https://doi.org/10.1523/JNEUROSCI.2279-19.2019 Copyright © 2020 Warren et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License Creative Commons Attribution 4.0 International, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
Funding Information:
This work was supported by the Royal Society and the Leverhulme Trust, by the Department of Neuroscience, Psychology, and Behavior Within the University of Leicester, and the Wellcome Trust Institutional Strategic Support Fund to B.W.; by a Royal Society Enhancement Award to G.F.; by the European Research Council under the European Union?s Seventh Framework Program (FP/2007-2013)/ERC Grant 615030 to E.K. and J.F.C.W.; and by Discovery Grant RGPIN/03712 from the Natural Sciences and Engineering Research Council of Canada to A.S.F. We thank Neil Rimmer and Jake Cranston for locust husbandry; Ben Cooper and Brendan O?Connor for help with statistical analysis and making sure the locust treatment remained blinded to the experimenter; and Nathan Suray for performing preliminary experiments for in vivo hook electrode recordings.
Publisher Copyright:
Copyright © 2020 Warren et al.
ASJC Scopus Subject Areas
- General Neuroscience