Drosophila adults exposed to acoustic trauma have been assessed for changes in auditory function and structure. Immediate effects on auditory function are observed, with reduced and delayed evoked activity. Although evoked potential amplitudes are restored after 7 days, the latency of these potentials does not fully recover. No gross morphological changes in the auditory organ (Johnston's organ, JO) are detected, but significant changes in mitochondrial morphology of neurons of the Johnston's organ are observed. Drosophila exhibit acoustic trauma effects resembling those found in vertebrates, including inducing metabolic stress in sensory cells.
Mutant flies with a reduced copy number of nrv3, which encodes a beta subunit of the sodium-potassium pump and is expressed in neurons of the Johnston's organ, were assessed. Animals heterozygous for nrv3 show increased sensitivity to noise trauma and a significantly reduced auditory functional recovery, leading to the conclusion that compromised JO ionic homeostasis confers susceptibility to noise trauma.
[updated Nov. 2019 by FlyBase; FBrf0222196]
Sounds can be harmful when they are too loud, even for a brief time, or when they are both loud and long-lasting. These sounds can damage structures in the inner ear and cause noise-induced hearing loss (NIHL). NIHL can be immediate or it can take a long time to be noticeable. It can be temporary or permanent, and it can affect one ear or both ears (https://www.nidcd.nih.gov/health/noise-induced-hearing-loss).
Most NIHL is caused by the damage and eventual death of the hair cells in the inner ear (https://www.nidcd.nih.gov/health/noise-induced-hearing-loss).
Moderate- to high-scoring ortholog of human ATP1B1, ATP1B2, ansd ATP1B3 (multiple related genes in both species).
