ArticleThe Journal of experimental biology2014
Recovery of otoacoustic emissions after high-level noise exposure in the American bullfrog.
Article in The Journal of experimental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Cut through the noise: vocal signals and auditory processing vary along an urbanization gradient in Pacific treefrogs.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2026Article
- Single-cell atlas comparison across vertebrates reveals auditory cell evolution and mechanisms for hair cell regeneration.Communications biology · 2024Article
- The paradox of hearing at the lek: auditory sensitivity increases after breeding in female gray treefrogs (Hyla chrysoscelis).Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The American bullfrog (Rana catesbeiana) has an amphibian papilla (AP) that senses airborne, low-frequency sound and generates distortion product otoacoustic emissions (DPOAEs) similar to other vertebrate species. Although ranid frogs are typically found in noisy environments, the effects of noise on the AP have not been studied. First, we determined the noise levels that diminished DPOAE at 2f1-f2 using an f2 stimulus level at 80 dB SPL and that also produced morphological damage of the sensory epithelium. Second, we compared DPOAE (2f1-f2) responses with histopathologic changes occurring in bullfrogs after noise exposure. Consistent morphological damage, such as fragmented hair cells and missing bundles, as well as elimination of DPOAE responses were seen only after very high-level (>150 dB SPL) sound exposures. The morphological response of hair cells to noise differed along the mediolateral AP axis: medial hair cells were sensitive to noise and lateral hair cells were relatively insensitive to noise. Renewed or repaired hair cells were not observed until 9 days post-exposure. Following noise exposure, DPOAE responses disappeared within 24 h and then recovered to normal pre-exposure levels within 3-4 days. Our results suggest that DPOAEs in the bullfrog are sensitive to the initial period of hair cell damage. After noise-induced damage, the bullfrog AP has functional recovery mechanisms that do not depend on substantial hair cell regeneration or repair. Thus, the bullfrog auditory system might serve as an interesting model for investigation of ways to prevent noise damage.
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