Temperature dependence of distortion-product otoacoustic emissions in tympanal organs of locusts

Abstract

SUMMARY Distortion-product otoacoustic emissions (DPOAEs) in tympanal organs of insects are vulnerable to manipulations that interfere with the animal's physiological state. Starting at a medium temperature, we raised and lowered the locust's body temperature within the range of 12 to 35°C by changing the temperature of the surrounding air, while recording DPOAEs. These experimental manipulations resulted in reversible amplitude changes of the 2f1–f2 emission, which were dependent on stimulus frequency and level. Using low f2 frequencies of up to 10 kHz, a temperature increase (median +8–9°C) led to an upward shift of DPOAE amplitudes of approximately +10 dB, whereas a temperature decrease (median −7°C) was followed by a reduction of DPOAE amplitudes by 3 to 5 dB. Both effects were only present in the range of the low-level component of DPOAE growth functions below L2 levels (levels of the f2 stimulus) of approximately 30 dB SPL. DPOAEs evoked by higher stimulus levels as well as measurements using higher stimulation frequencies above 10 kHz remained unaffected by any temperature shifts. The Arrhenius activation energy was calculated from the −10 dB SPL thresholds (representing the low-level component) of growth functions, which had been measured with 8 and 10 kHz as f2 frequencies and amounted to up to ~34 and 41 kJ mol−1, respectively. Such activation energy values provide a hint that the dynein-tubulin system within the scolopidial receptors could play an essential part in the DPOAE generation in tympanal organs.

Bridging the Gap Between Mammal and Insect Ears – A Comparative and Evolutionary View of Sound-Reception

“…As insect auditory cilia have a microtubule cytoskeleton bearing dynein arms (Karak et al, 2015), channel closing in insects is thought to be powered by dynein (see for review Göpfert and Robert, 2008;Göpfert and Hennig, 2016; Figure 2Cii). Further supporting dynein's role in transduction, are measurements of the temperature dependence of spontaneous oscillations in mosquitoes (Warren et al, 2010), and distortion-product otoacoustic emissions in locusts (Möckel et al, 2012) both hallmarks of the transduction process. The temperature dependence of biological processes gives information about the chemical reactions that produce them.…”

What can insects teach us about hearing loss?

“…Nevertheless, the nature of sound and the challenges of sound localization, selection and often the amplification of relevant signals from background are common problems, and nature has solved many of these problems in different but parallel ways. For example, amplification mechanisms involve both shared and unique features between flies and mammals, in that the force of transduction channel closing altering gating compliance can provide an energy source for amplification in both systems (Howard & Hudspeth, 1988;Nadrowski et al, 2008), whereas motility-based sources involve Prestin electromotility in mammals (Zheng et al, 2000) but (presumably) ciliary dynein motility in insects (Karak et al, 2015;Kavlie et al, 2010;Möckel et al, 2012;Warren et al, 2010). Physiological hearing disorders are also caused by dysfunction of other ion channels, such as the voltage-gated Na + and K + channel in insects (Ravenscroft et al, 2023;Zhang, 2023) and K + channels and Ca 2+ channels in mammals (Baig et al, 2011;Kharkovets et al, 2000Kharkovets et al, , 2006Kubisch et al, 1999;Neyroud et al, 1997;Schulze-Bahr et al, 1997).…”

Mechanical tuning of the moth ear: distortion-product otoacoustic emissions and tympanal vibrations

“…Unresolved, however, is whether nonlinear sound amplification in the insect is due to active or passive cellular mechanisms. Cumulative evidence in moths, locusts and bushcrickets points to active cellular mechanisms to be partly responsible for the generation of DPOAE in tympanal organs in specific frequency ranges, with two main lines of evidence: (1) experimental manipulations that affect the physiological state of the animal, such as the application of certain anesthetics or hypoxic substances or cooling, also affect the insect's DPOAE (Kössl and Boyan, 1998a;Kössl and Boyan, 1998b;Kössl et al, 2007;Kössl et al, 2008;Möckel et al, 2011;Möckel et al, 2012); and (2) electrical or mechanical manipulation of sensory neurons causes changes in DPOAE amplitude (Möckel et al, 2007). Both lines of evidence suggest that the mechanosensitive neurones, which attach to the tympanum in moths and the locust but not in the bushcrickets, are the most likely candidate for the production of DPOAE in insects.…”