This paper tests key predictions of the "two-mechanism model" for the generation of distortion-product otoacoustic emissions (DPOAEs). The two-mechanism model asserts that lower-sideband DPOAEs constitute a mixture of emissions arising not simply from two distinct cochlear locations (as is now well established) but, more importantly, by two fundamentally different mechanisms: nonlinear distortion induced by the traveling wave and linear coherent reflection off pre-existing micromechanical impedance perturbations. The model predicts that (1) DPOAEs evoked by frequency-scaled stimuli (e.g., at fixed f2/f1) can be unmixed into putative distortion- and reflection-source components with the frequency dependence of their phases consistent with the presumed mechanisms of generation; (2) The putative reflection-source component of the total DPOAE closely matches the reflection-source emission (e.g., low level stimulus-frequency emission) measured at the same frequency under similar conditions. These predictions were tested by unmixing DPOAEs into components using two completely different methods: (a) selective suppression of the putative reflection source using a third tone near the distortion-product frequency and (b) spectral smoothing (or, equivalently, time-domain windowing). Although the two methods unmix in very different ways, they yield similar DPOAE components. The properties of the two DPOAE components are consistent with the predictions of the two-mechanism model.

Kalluri R, Xue J, Eatock RA. Ion channels set spike timing regularity of mammalian vestibular afferent neurons. J Neurophysiol 104: 2034-2051, 2010. First published July 21, 2010 doi:10.1152/jn.00396.2010. In the mammalian vestibular nerve, some afferents have highly irregular interspike intervals and others have highly regular intervals. To investigate whether spike timing is determined by the afferents' ion channels, we studied spiking activity in their cell bodies, isolated from the vestibular ganglia of young rats. Whole cell recordings were made with the perforated-patch method. As previously reported, depolarizing current steps revealed distinct firing patterns. Transient neurons fired one or two onset spikes, independent of current level. Sustained neurons were more heterogeneous, firing either trains of spikes or a spike followed by large voltage oscillations. We show that the firing pattern categories are robust, occurring at different temperatures and ages, both in mice and in rats. A difference in average resting potential did not cause the difference in firing patterns, but contributed to differences in afterhyperpolarizations. A low-voltage-activated potassium current (I LV ) was previously implicated in the transient firing pattern. We show that I LV grew from the first to second postnatal week and by the second week comprised Kv1 and Kv7 (KCNQ) components. Blocking I LV converted step-evoked firing patterns from transient to sustained. Separated from their normal synaptic inputs, the neurons did not spike spontaneously. To test whether the firing-pattern categories might correspond to afferent populations of different regularity, we injected simulated excitatory postsynaptic currents at pseudorandom intervals. Sustained neurons responded to a given pattern of input with more regular firing than did transient neurons. Pharmacological block of I LV made firing more regular. Thus ion channel differences that produce transient and sustained firing patterns in response to depolarizing current steps can also produce irregular and regular spike timing.

Otoacoustic emissions (OAEs) evoked by broadband clicks and by single tones are widely regarded as originating via different mechanisms within the cochlea. Whereas the properties of stimulus-frequency OAEs (SFOAEs) evoked by tones are consistent with an origin via linear mechanisms involving coherent wave scattering by preexisting perturbations in the mechanics, OAEs evoked by broadband clicks (CEOAEs) have been suggested to originate via nonlinear interactions among the different frequency components of the stimulus (e.g., intermodulation distortion). The experiments reported here test for bandwidth-dependent differences in mechanisms of OAE generation. Click-evoked and stimulus-frequency OAE input/output transfer functions were obtained and compared as a function of stimulus frequency and intensity. At low and moderate intensities human CEOAE and SFOAE transfer functions are nearly identical. When stimulus intensity is measured in "bandwidth-compensated" sound-pressure level (cSPL), CEOAE and SFOAE transfer functions have equivalent growth functions at fixed frequency and equivalent spectral characteristics at fixed intensity. This equivalence suggests that CEOAEs and SFOAEs are generated by the same mechanism. Although CEOAEs and SFOAEs are known by different names because of the different stimuli used to evoke them, the two OAE "types" are evidently best understood as members of the same emission family.