Katrin Krumbholz

The auditory system decomposes sounds into different frequencies, but does not represent them equally: in the human cochlea, lower frequencies occupy a larger spatial extent than higher frequencies, creating a quasi-logarithmic frequency map with finer low-frequency resolution. It remains unclear whether the primary auditory cortex preserves this quasi-logarithmic frequency mapping, or further magnifies behaviourally relevant frequencies, analogous to the foveal over-magnification in primary visual cortex that is thought to underpin visual hyperacuity phenomena such as Vernier acuity. Here, we used ultra-high field functional magnetic resonance imaging to quantify frequency magnification in the primary auditory cortex of 20 human listeners. We compared cortical frequency magnification to predictions based on published estimates of either cochlear frequency resolution or behavioural frequency discrimination performance, a form of perceptual frequency hyperacuity. Cortical frequency magnification was better predicted by frequency discrimination performance than by cochlear frequency resolution, with an additional unexpected over-representation of frequencies around 1 kHz. These findings suggest that frequency discrimination is constrained by cortical processes rather than by frequency information available at the cochlea, consistent with similar observations in the visual and tactile systems.

Tonotopy is a fundamental feature of auditory cortical organization, yet its influence on cortical auditory-evoked responses (AERs) remains unclear. Consequently, key properties of cortical AERs—such as their marked amplitude reduction with increasing stimulus frequency—still lack a coherent mechanistic explanation. To address this gap, we combined a meta-analysis of frequency-specific AER amplitudes with forward simulations of AERs informed by current knowledge of auditory cortical tonotopic layout and functional organization. The meta-analysis used a semi-systematic search covering all known automatic cortical AER components—both transient-evoked and steady-state—along with selected subcortical components for comparison. Forward simulations were based on a functional parcellation of the human supratemporal auditory region into subdivisions forming distinct tonotopic maps, and an idealized model of each division's intrinsic tonotopic layout. Parcellation was achieved using a novel, largely automated procedure applied to high-field (3 T) and ultra-high-field (7 T) functional and microstructural MRI mapping data from 30 individual hemispheres. Meta-analytic results revealed that, whilst all cortical AER components consistently show frequency-related amplitude reduction, reduction is greater in steady-state compared to transient-evoked components. Simulations indicated that frequency-related amplitude reduction arising from cortical morphology is confined to the highly myelinated central portion of Heschl's gyrus, suggesting that differences in reduction amount between steady-state and transient-evoked components may reflect differences in the relative strengths of their primary contributions. Our findings provide a new perspective on cortical AER generation. They represent an important step toward explaining morphology-related variability in AER amplitudes and establishing a quantitative link to underlying source strengths.

Auditory brainstem responses (ABRs) to broadband clicks are strongly affected by dyssynchrony, or “latency dispersion”, of their frequency-specific cochlear contributions. Optimized chirp stimuli, designed to compensate for cochlear dispersion, can afford substantial increase in broadband ABR amplitudes, particularly for the prominent wave-V deflection. Reports on the smaller wave I, however, which may be useful for measuring cochlear synaptopathy, have been mixed. This study aimed to test previous claims that ABR latency dispersion differs between waves I and V, and between males and females, and thus that using wave- and/or sex-tailored chirps may provide more reliable wave-I benefit. Using the derived-band technique, we measured responses from frequency-restricted (one-octave-wide) cochlear regions to energy-matched click and chirp stimuli. The derived-band responses’ latencies were used to assess any wave- and/or sex-related dispersion differences across bands, and their amplitudes, to evaluate any within-band dispersion differences. Our results suggest that sex-related dispersion difference within the lowest-frequency cochlear regions (< 1 kHz), where dispersion is generally greatest, may be a predominant driver of the often-reported sex difference in broadband ABR amplitude. At the same time, they showed no systematic dispersion difference between waves I and V. Instead, they suggest that reduced chirp benefit on wave I may arise as a result of chirp-induced desynchronization of on- and off-frequency responses generated at the same cochlear places, and resultant reduction in response contributions from higher-frequency cochlear regions, to which wave I is thought to be particularly sensitive.

Measuring neuronal frequency selectivity in human auditory cortex may be crucial for understanding common auditory deficits such as speech-in-noise difficulty. Non-invasive methods measure aggregate responses of large populations of neurons and therefore overestimate single-neuron tuning selectivity. Here we explore whether cortical frequency selectivity can be estimated through fMRI adaptation. Using ultra-high-field (7T) BOLD-fMRI and individualized functional parcellation of auditory cortex, we measured the suppression (or adaptation) of primary and non-primary cortical responses to a high-frequency (3.8 kHz) probe sound as a function of the frequency of a preceding adaptor sound (ranging from 0.5 to 3.8 kHz). The degree of frequency tuning of the adaptation effect strongly depended on the temporal structure of the adaptor. Suppression by a single 200-ms adaptor showed little or no tuning, despite clear frequency tuning of the responses to the different adaptors. In contrast, suppression by multiple (four) 50-ms adaptor bursts was clearly tuned, with greater frequency selectivity than the adaptor response tuning, suggesting that fMRI adaption to multiple adaptors may reflect the frequency tuning of the underlying neuronal response. Importantly, adaptation tuning differed between primary and non-primary regions, suggesting a local suppression effect, rather than inheritance from upstream subcortical structures. Using a computational model of fMRI adaptation in a tonotopically-organized neuronal array, we identify key factors determining the relationship between observed fMRI adaptation tuning and the frequency selectivity of the underlying neuronal response. Using this model, we derive a plausible range for the frequency selectivity of individual neurons in each region of auditory cortex.

It is commonly assumed that difficulty in listening to speech in noise is at least partly due to deficits in neural temporal processing. Given that noise reduces the temporal fidelity of the auditory brainstem response (ABR) to speech, it has been suggested that the speech ABR may serve as an index of such neural deficits. However, the temporal fidelity of ABRs, to both speech and non-speech sounds, is also known to be influenced by the cochlear origin of the response, as responses from higher-frequency cochlear regions are faster and more synchronous than responses from lower-frequency regions. Thus, if noise caused a reweighting of response contributions from higher- to lower-frequency cochlear regions, the temporal fidelity of the aggregate response should be reduced even in the absence of any changes in neural processing. This ‘place mechanism’ has been demonstrated for non-speech ABRs. The aim of this study was to test whether it also applies to speech ABRs. We used the so-called ‘derived-band’ method to isolate response contributions from frequency-limited cochlear regions. Broadband and derived-band speech ABRs were measured both in quiet and in noise. Whilst the noise caused significant changes to the temporal properties of the broadband response, its effects on the derived-band responses were mostly restricted to the response amplitudes. Importantly, the amplitudes of the higher-frequency derived-band responses were much more strongly affected than those of the lower-frequency responses, suggesting that the noise indeed caused a reweighting effect. Our results indicate that, as for non-speech ABRs, the cochlear place mechanism can represent a potentially substantial confound to speech-ABR-in-noise measurements.

Previous findings have suggested that auditory attention causes not only enhancement in neural processing gain, but also sharpening in neural frequency tuning in human auditory cortex. The current study was aimed to reexamine these findings. Specifically, we aimed to investigate whether attentional gain enhancement and frequency sharpening emerge at the same or different processing levels and whether they represent independent or cooperative effects. For that, we examined the pattern of attentional modulation effects on early, sensory-driven cortical auditory-evoked potentials occurring at different latencies. Attention was manipulated using a dichotic listening task and was thus not selectively directed to specific frequency values. Possible attention-related changes in frequency tuning selectivity were measured with an adaptation paradigm. Our results show marked disparities in attention effects between the earlier N1 deflection and the subsequent P2 deflection, with the N1 showing a strong gain enhancement effect, but no sharpening, and the P2 showing clear evidence of sharpening, but no independent gain effect. They suggest that gain enhancement and frequency sharpening represent successive stages of a cooperative attentional modulation mechanism that increases the representational bandwidth of attended versus unattended sounds.

The active cochlear mechanism amplifies responses to low-intensity sounds, compresses the range of input sound intensities to a smaller output range, and increases cochlear frequency selectivity. The gain of the active mechanism can be modulated by the medial olivocochlear (MOC) efferent system, creating the possibility of top-down control at the earliest level of auditory processing. In humans, MOC function has mostly been measured by the suppression of otoacoustic emissions (OAEs), typically as a result of MOC activation by a contralateral elicitor sound. The exact relationship between OAE suppression and cochlear gain reduction, however, remains unclear. Here, we measured the effect of a contralateral MOC elicitor on perceptual estimates of cochlear gain and compression, obtained using the established temporal masking curve (TMC) method. The measurements were taken at a signal frequency of 2 kHz and compared with measurements of click-evoked OAE suppression. The elicitor was a broadband noise, set to a sound pressure level of 54 dB to avoid triggering the middle ear muscle reflex. Despite its low level, the elicitor had a significant effect on the TMCs, consistent with a reduction in cochlear gain. The amount of gain reduction was estimated as 4.4 dB on average, corresponding to around 18 % of the without-elicitor gain. As a result, the compression exponent increased from 0.18 to 0.27.

Electrophysiological and psychophysical responses to a low-intensity probe sound tend to be suppressed by a preceding high-intensity adaptor sound. Nevertheless, rare low-intensity deviant sounds presented among frequent high-intensity standard sounds in an intensity oddball paradigm can elicit an electroencephalographic mismatch negativity (MMN) response. This has been taken to suggest that the MMN is a correlate of true change or “deviance” detection. A key question is where in the ascending auditory pathway true deviance sensitivity first emerges. Here, we addressed this question by measuring low-intensity deviant responses from single units in the inferior colliculus (IC) of anesthetized rats. If the IC exhibits true deviance sensitivity to intensity, IC neurons should show enhanced responses to low-intensity deviant sounds presented among high-intensity standards. Contrary to this prediction, deviant responses were only enhanced when the standards and deviants differed in frequency. The results could be explained with a model assuming that IC neurons integrate over multiple frequency-tuned channels and that adaptation occurs within each channel independently. We used an adaptation paradigm with multiple repeated adaptors to measure the tuning widths of these adaption channels in relation to the neurons’ overall tuning widths.

The speech-evoked auditory brain stem response (speech ABR) is widely considered to provide an index of the quality of neural temporal encoding in the central auditory pathway. The aim of the present study was to evaluate the extent to which the speech ABR is shaped by spectral processing in the cochlea. High-pass noise masking was used to record speech ABRs from delimited octave-wide frequency bands between 0.5 and 8 kHz in normal-hearing young adults. The latency of the frequency-delimited responses decreased from the lowest to the highest frequency band by up to 3.6 ms. The observed frequency-latency function was compatible with model predictions based on wave V of the click ABR. The frequency-delimited speech ABR amplitude was largest in the 2- to 4-kHz frequency band and decreased toward both higher and lower frequency bands despite the predominance of low-frequency energy in the speech stimulus. We argue that the frequency dependence of speech ABR latency and amplitude results from the decrease in cochlear filter width with decreasing frequency. The results suggest that the amplitude and latency of the speech ABR may reflect interindividual differences in cochlear, as well as central, processing. The high-pass noise-masking technique provides a useful tool for differentiating between peripheral and central effects on the speech ABR. It can be used for further elucidating the neural basis of the perceptual speech deficits that have been associated with individual differences in speech ABR characteristics.