The encoding of temporal regularities is a critical property of the auditory system, as short-term neural representations of environmental statistics serve to auditory object formation and detection of potentially relevant novel stimuli. A putative neural mechanism underlying regularity encoding is repetition suppression, the reduction of neural activity to repeated stimulation. Although repetitive stimulation per se has shown to reduce auditory neural activity in animal cortical and subcortical levels and in the human cerebral cortex, other factors such as timing may influence the encoding of statistical regularities. This study was set out to investigate whether temporal predictability in the ongoing auditory input modulates repetition suppression in subcortical stages of the auditory processing hierarchy. Human auditory frequency–following responses (FFR) were recorded to a repeating consonant–vowel stimuli (/wa/) delivered in temporally predictable and unpredictable conditions. FFR amplitude was attenuated by repetition independently of temporal predictability, yet we observed an accentuated suppression when the incoming stimulation was temporally predictable. These findings support the view that regularity encoding spans across the auditory hierarchy and point to temporal predictability as a modulatory factor of regularity encoding in early stages of the auditory pathway.

The mismatch negativity (MMN) provides a correlate of automatic auditory discrimination in human auditory cortex that is elicited in response to violation of any acoustic regularity. Recently, deviance-related responses were found at much earlier cortical processing stages as reflected by the middle latency response (MLR) of the auditory evoked potential, and even at the level of the auditory brainstem as reflected by the frequency following response (FFR). However, no study has reported deviance-related responses in the FFR, MLR and long latency response (LLR) concurrently in a single recording protocol. Amplitude-modulated (AM) sounds were presented to healthy human participants in a frequency oddball paradigm to investigate deviance-related responses along the auditory hierarchy in the ranges of FFR, MLR and LLR. AM frequency deviants modulated the FFR, the Na and Nb components of the MLR, and the LLR eliciting the MMN. These findings demonstrate that it is possible to elicit deviance-related responses at three different levels (FFR, MLR and LLR) in one single recording protocol, highlight the involvement of the whole auditory hierarchy in deviance detection and have implications for cognitive and clinical auditory neuroscience. Moreover, the present protocol provides a new research tool into clinical neuroscience so that the functional integrity of the auditory novelty system can now be tested as a whole in a range of clinical populations where the MMN was previously shown to be defective.

A flourishing line of evidence has highlighted the encoding of speech sounds in the subcortical auditory system as being shaped by acoustic, linguistic, and musical experience and training. And while the heritability of auditory speech as well as nonspeech processing has been suggested, the genetic determinants of subcortical speech processing have not yet been uncovered. Here, we postulated that the serotonin transporter-linked polymorphic region (5-HTTLPR), a common functional polymorphism located in the promoter region of the serotonin transporter gene (SLC6A4), is implicated in speech encoding in the human subcortical auditory pathway. Serotonin has been shown as essential for modulating the brain response to sound both cortically and subcortically, yet the genetic factors regulating this modulation regarding speech sounds have not been disclosed. We recorded the frequency following response, a biomarker of the neural tracking of speech sounds in the subcortical auditory pathway, and cortical evoked potentials in 58 participants elicited to the syllable /ba/, which was presented Ͼ2000 times. Participants with low serotonin transporter expression had higher signal-to-noise ratios as well as a higher pitch strength representation of the periodic part of the syllable than participants with medium to high expression, possibly by tuning synaptic activity to the stimulus features and hence a more efficient suppression of noise. These results imply the 5-HTTLPR in subcortical auditory speech encoding and add an important, genetically determined layer to the factors shaping the human subcortical response to speech sounds.

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Attention capture by potentially relevant environmental stimuli is critical for human survival, yet it varies considerably among individuals. A large series of studies has suggested that attention capture may depend on the cognitive balance between maintenance and manipulation of mental representations and the flexible switch between goal-directed representations and potentially relevant stimuli outside the focus of attention; a balance that seems modulated by a prefrontostriatal dopamine pathway. Here, we examined inter-individual differences in the cognitive control of attention through studying the effects of two single nucleotide polymorphisms regulating dopamine at the prefrontal cortex and the striatum (i.e., COMTMet108/158Val and ANKK1/DRD2TaqIA) on stimulus-driven attention capture. Healthy adult participants (N = 40) were assigned to different groups according to the combination of the polymorphisms COMTMet108/158Val and ANKK1/DRD2TaqIA, and were instructed to perform on a well-established distraction protocol. Performance in individuals with a balance between prefrontal dopamine display and striatal receptor density was slowed down by the occurrence of unexpected distracting events, while those with a rather unbalanced dopamine activity were able maintain task performance with no time delay, yet at the expense of a slightly lower accuracy. This advantage, associated to their distinct genetic profiles, was paralleled by an electrophysiological mechanism of phase-resetting of gamma neural oscillation to the novel, distracting events. Taken together, the current results suggest that the epistatic interaction between COMTVal108/158Met and ANKK1/DRD2 TaqIa genetic polymorphisms lies at the basis of stimulus-driven attention capture.

Auditory deviance detection based on regularity encoding appears as one of the basic functional properties of the auditory system. It has traditionally been assessed with the mismatch negativity (MMN) long-latency component of the auditory evoked potential (AEP). Recent studies have found earlier correlates of deviance detection based on regularity encoding. They occur in humans in the first 50 ms after sound onset, at the level of the middle-latency response of the AEP, and parallel findings of stimulus-specific adaptation observed in animal studies. However, the functional relationship between these different levels of regularity encoding and deviance detection along the auditory hierarchy has not yet been clarified. Here we addressed this issue by examining deviant-related responses at different levels of the auditory hierarchy to stimulus changes varying in their degree of deviation regarding the spatial location of a repeated standard stimulus. Auditory stimuli were presented randomly from five loudspeakers at azimuthal angles of 0°, 12°, 24°, 36° and 48° during oddball and reversed-oddball conditions. Middle-latency responses and MMN were measured. Our results revealed that middle-latency responses were sensitive to deviance but not the degree of deviation, whereas the MMN amplitude increased as a function of deviance magnitude. These findings indicated that acoustic regularity can be encoded at the level of the middle-latency response but that it takes a higher step in the auditory hierarchy for deviance magnitude to be encoded, thus providing a functional dissociation between regularity encoding and deviance detection along the auditory hierarchy.

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