Biomechanical alterations following acoustic trauma in Schistocerca gregaria

Noise-induced hearing loss (NIHL) is known to be caused by long exposures to intense acoustic stimuli, yet very little is known of the mechanical and physiological mechanisms involved in this form of acoustic trauma. In humans, typical symptoms of this condition range from intra- and extracellular structural disruptions to total sensory cell damage or loss, which lead to permanent damage or complete hearing loss. Investigations of acoustic trauma in Drosophila melanogaster found that deafened individuals displayed altered sound-evoked potentials (SEPs) and mitochondrial morphology, and that those symptoms were further enhanced in mutants when sensory cell ion homeostasis was compromised. However, no obvious anatomical alterations were noted, suggesting that in drosophila NIHL is primarily a product of physiological dysfunction in the sensory cells (Christie et al., 2013).
Further investigating the mechanisms underlying NIHL in insects, this study used deafened locusts Schistocerca gregaria and recorded the tympanal mechanical behaviour of individuals exposed to intense stimuli of various frequencies. Results show that the mechanical gain of the tympanal membrane increased post-trauma. Yet, current electrophysiological investigations of scolopidial transduction in deafened locusts suggest that transduction is severely reduced or even altogether absent following acoustic trauma (B. Warren, unpublished data). In addition to supporting the etiology of acoustic trauma in other species, such an investigation therefore also clarifies the role of sensory cells in signal amplification and filtering in the tympanal organs of Caeliferans.