Sensitive hearing organs often employ nonlinear mechanical sound processing which generates distortion-product otoacoustic emissions (DPOAE). Such emissions are also recordable from tympanal organs of insects. In vertebrates (including humans), otoacoustic emissions are considered by-products of active sound amplification through specialized sensory receptor cells in the inner ear. Force generated by these cells primarily augments the displacement amplitude of the basilar membrane and thus increases auditory sensitivity. As in vertebrates, the emissions from insect ears are based on nonlinear mechanical properties of the sense organ. Apparently, to achieve maximum sensitivity, convergent evolutionary principles have been realized in the micromechanics of these hearing organs-although vertebrates and insects possess quite different types of receptor cells in their ears. Just as in vertebrates, otoacoustic emissions from insects ears are vulnerable and depend on an intact metabolism, but so far in tympanal organs, it is not clear if auditory nonlinearity is achieved by active motility of the sensory neurons or if passive cellular characteristics cause the nonlinear behavior. In the antennal ears of flies and mosquitoes, however, active vibrations of the flagellum have been demonstrated. Our review concentrates on experiments studying the tympanal organs of grasshoppers and moths; we show that their otoacoustic emissions are produced in a frequency-specific way and can be modified by electrical stimulation of the sensory cells. Even the simple ears of notodontid moths produce distinct emissions, although they have just one auditory neuron. At present it is still uncertain, both in vertebrates and in insects, if the nonlinear amplification so essential for sensitive sound processing is primarily due to motility of the somata of specialized sensory cells or to active movement of their (stereo-)cilia. We anticipate that further experiments with the relatively simple ears of insects will help answer these questions.

Bushcrickets have a tonotopically organised hearing organ, the so-called crista acustica, in the tibia of the forelegs. This organ responds to a frequency range of about 5-80 kHz and lies behind the anterior tympanum on top of a trachea branch. We analyzed the sound-induced vibration pattern of the anterior tympanum, using a Laser-Doppler-Vibrometer Scanning microscope system, in order to identify frequency-dependent amplitude and phase of displacement. The vibration pattern evoked by a frequency sweep (4-79 kHz) showed an amplitude maximum which would correspond to the resonance frequency of an open tube system. At higher frequencies of about 30 kHz a difference in the amplitude and phase response between the distal and the proximal part of the tympanum was detected. The inner plate of the tympanum starts to wobble at this frequency. This higher mode in the motion pattern is not explained by purely acoustic characteristics of the tracheal space below the tympanum but may depend on the mechanical impedance of the tympanum plate. In accordance with a previous hypothesis, the tympanum moves over the whole tested frequency range in the dorso-ventral direction like a hinged flap with the largest displacement in its ventral part and no higher modes of vibration.

Tympanal organs of insects emit distortion-product otoacoustic emissions (DPOAEs) that are indicative of nonlinear ear mechanics. Our study sought (1) to define constraints of DPOAE generation in the ear of Locusta migratoria, and (2) to identify the sensory structures involved. We selectively destroyed the connection between the (peripheral) sensory ganglion and the tympanal attachment points of the "d-cell" dendrites; d-cells are most sensitive to sound frequencies above 12 kHz. This led to a decrease of DPOAEs that were evoked by f (2) frequencies above 15 kHz (decrease of 15-40 dB; mean 28 dB; n = 12 organs). DPOAEs elicited by lower frequencies remained unchanged. Such frequency-specific changes following the exclusion of one scolopidial sub-population suggest that these auditory scolopidia are in fact the source of DPOAEs in insects. Electrical stimulation of the auditory nerve (with short current pulses of 4-10 microA or DC-currents of 0.5 microA) reversibly reduced DPOAEs by as much as 30 dB. We assume that retrograde electrical stimulation primarily affected the neuronal part of the scolopidia. Severing the auditory nerve from the central nervous system (CNS) did not alter the DPOAE amplitudes nor the effects of electrical stimulation.

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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