Abstract
The tympanal organ of the bushcricket Mecopoda elongata emits pronounced distortion-product otoacoustic emissions (DPOAEs). Their characteristics are comparable to those measured in other insects, such as locusts and moths, with the 2f1-f2 emission being the most prominent one. Yet the site of their generation is still unclear. The spatial separation between the sound receiving spiracle and the hearing organ in this species allows manipulations of the sensory cells without interfering with the acoustical measurements. We tried to interfere with the DPOAE generation by pharmacologically influencing the tympanal organ using the insecticide pymetrozine. The compound appears to act selectively on scolopidia, i.e., the mechanosensor type characteristically constituting tympanal organs. Pymetrozine solutions were applied as closely as possible to the scolopidia via a cuticle opening in the tibia, distally to the organ. Applications of pymetrozine at concentrations between 10(-3) and 10(-7)M to the tympanal organ led to a pronounced and irreversible decrease of the DPOAE amplitudes.
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