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Alignment of neural oscillations with temporally regular input allows listeners to generate temporal expectations. However, it remains unclear how behavior is governed in the context of temporal variability: What role do temporal expectations play, and how do they interact with the strength of neural oscillatory activity? Here, human participants detected near-threshold targets in temporally variable acoustic sequences. Temporal expectation strength was estimated using an oscillator model and pre-target neural amplitudes in auditory cortex were extracted from magnetoencephalography signals. Temporal expectations modulated target-detection performance, however, only when neural delta-band amplitudes were large. Thus, slow neural oscillations act to gate influences of temporal expectation on perception. Furthermore, slow amplitude fluctuations governed linear and quadratic influences of auditory alpha-band activity on performance. By fusing a model of temporal expectation with neural oscillatory dynamics, the current findings show that human perception in temporally variable contexts relies on complex interactions between multiple neural frequency bands. •Slow neural oscillations act to gate influences of temporal expectation on perception.•Alpha oscillations in auditory cortex affect auditory perception.•Auditory alpha-band influences on perception depend on delta-band amplitude.

Tau rhythms are largely defined by sound responsive alpha band (~8–13 Hz) oscillations generated largely within auditory areas of the superior temporal gyri. Studies of tau have mostly employed magnetoencephalography or intracranial recording because of tau's elusiveness in the electroencephalogram. Here, we demonstrate that independent component analysis (ICA) decomposition can be an effective way to identify tau sources and study tau source activities in EEG recordings. Subjects (N = 18) were passively exposed to complex acoustic stimuli while the EEG was recorded from 68 electrodes across the scalp. Subjects' data were split into 60 parallel processing pipelines entailing use of five levels of high‐pass filtering (passbands of 0.1, 0.5, 1, 2, and 4 Hz), three levels of low‐pass filtering (25, 50, and 100 Hz), and four different ICA algorithms (fastICA, infomax, adaptive mixture ICA [AMICA], and multi‐model AMICA [mAMICA]). Tau‐related independent component (IC) processes were identified from this data as being localized near the superior temporal gyri with a spectral peak in the 8–13 Hz alpha band. These “tau ICs” showed alpha suppression during sound presentations that was not seen for other commonly observed IC clusters with spectral peaks in the alpha range (e.g., those associated with somatomotor mu, and parietal or occipital alpha). The choice of analysis parameters impacted the likelihood of obtaining tau ICs from an ICA decomposition. Lower cutoff frequencies for high‐pass filtering resulted in significantly fewer subjects showing a tau IC than more aggressive high‐pass filtering. Decomposition using the fastICA algorithm performed the poorest in this regard, while mAMICA performed best. The best combination of filters and ICA model choice was able to identify at least one tau IC in the data of ~94% of the sample. Altogether, the data reveal close similarities between tau EEG IC dynamics and tau dynamics observed in MEG and intracranial data. Use of relatively aggressive high‐pass filters and mAMICA decomposition should allow researchers to identify and characterize tau rhythms in a majority of their subjects. We believe adopting the ICA decomposition approach to EEG analysis can increase the rate and range of discoveries related to auditory responsive tau rhythms. Auditory related alpha rhythms (i.e., tau rhythms) have historically been difficult to examine with the electroencephalogram (EEG). Here, we show that independent components analysis, combined with the right preprocessing routines, can be an effective way to examine tau rhythms in the EEG.

Although widely used, no proof exists for the feasibility of neurofeedback for reinstating the disordered excitatory–inhibitory balance, marked by a decrease in auditory alpha power, in tinnitus patients. The current study scrutinizes the ability of neurofeedback to focally increase alpha power in auditory areas in comparison to the more common rTMS. Resting-state MEG was measured before and after neurofeedback ( n  = 8) and rTMS ( n  = 9) intervention respectively. Source level power and functional connectivity were analyzed with a focus on the alpha band. Only neurofeedback produced a significant decrease in tinnitus symptoms and—more important for the context of the study—a spatially circumscribed increase in alpha power in right auditory regions. Connectivity analysis revealed higher outgoing connectivity in a region ultimately neighboring the area in which power increases were observed. Neurofeedback decreases tinnitus symptoms and increases alpha power in a spatially circumscribed manner. In addition, compared to a more established brain stimulation-based intervention, neurofeedback is a promising approach to renormalize the excitatory–inhibitory imbalance putatively underlying tinnitus. This study is the first to demonstrate the feasibility of focally enhancing alpha activity in tinnitus patients by means of neurofeedback.

The sensorimotor dorsal stream is known to activate in both overt and covert speech production. However, overt production produces sensory consequences that are absent during covert production. Thus, the purpose of the current study is to investigate differences in dorsal stream activity between these two production conditions across the time course of utterances. Electroencephalography (EEG) was recorded from 68 channels while 23 participants overtly (Op) and covertly (Cp) produced orthographically cued bisyllabic targets. Sensorimotor mu and auditory alpha components (from anterior and posterior aspects of the dorsal stream) were identified using independent component analysis (ICA). Event-related spectral perturbation (ERSP) analyses identified changes in mu and alpha oscillatory power over time, while intercomponent phase coherence (IPC) measured anterior–posterior connectivity in the two conditions. Results showed greater beta (15–25 Hz) suppression during speech planning across left and right hemisphere sensorimotor and temporal ICs for Op relative to Cp. By contrast, greater intrahemispheric beta coherence was observed for Cp compared to Op during speech planning. During execution, greater beta suppression was observed along with greater low frequency (< 10 Hz) power enhancement and intrahemispheric phase coherence in Op compared to Cp. The findings implicate low frequency sensorimotor and posterior temporal phase coherence in the integration of somatosensory and acoustic feedback in overt relative to covert execution. Findings are consistent with early frontal–temporal forward models involved in planning and execution with modulations depending on whether the task goal is internal or overt syllable production.

Increasing evidence underlines the functional importance of non-phase-locked cortical oscillatory rhythms. Among the different oscillations, alpha (8–12Hz) has been shown to be modulated by anticipation or attention, suggesting a top-down influence. However, most studies to date have been conducted in the visual modality and the extent to which this notion also applies to the auditory cortex is unclear. It is furthermore often difficult to dissociate bottom-up from top-down contributions in cases of different stimuli (e.g., standards vs. deviants) or stimuli that are preceded by different cues. This study addresses these issues by investigating neuronal responses associated with intrinsically fluctuating perceptions of an invariant sound. Sixteen participants performed a pseudo-frequency-discrimination task in which a “high-pitch” tone was followed by an aversive noise, while the “low-pitch” tone was followed by silence. The participants had to decide which tone was presented even though the stimulus was actually kept constant while pseudo-randomized feedback was given. EEG data show that auditory cortical alpha power decreased by 20% in “high-pitch” trials relative to trials in which a “low pitch” was perceived. This study shows that expectancy of aversive feedback modulates perception of sounds and these fluctuating perceptions become manifest in modulations of sound-related alpha desynchronizations. Our findings extend recent evidence in the visual and somatosensory domain that alpha oscillations represent the excitatory/inhibitory balance of sensory cortical cell assemblies, which can be tuned in a top-down manner.

Sensorimotor integration (SMI) across the dorsal stream enables online monitoring of speech. Jenson et al. (2014) used independent component analysis (ICA) and event related spectral perturbation (ERSP) analysis of electroencephalography (EEG) data to describe anterior sensorimotor (e.g., premotor cortex, PMC) activity during speech perception and production. The purpose of the current study was to identify and temporally map neural activity from posterior (i.e., auditory) regions of the dorsal stream in the same tasks. Perception tasks required \"active\" discrimination of syllable pairs (/ba/ and /da/) in quiet and noisy conditions. Production conditions required overt production of syllable pairs and nouns. ICA performed on concatenated raw 68 channel EEG data from all tasks identified bilateral \"auditory\" alpha (α) components in 15 of 29 participants localized to pSTG (left) and pMTG (right). ERSP analyses were performed to reveal fluctuations in the spectral power of the α rhythm clusters across time. Production conditions were characterized by significant α event related synchronization (ERS; pFDR < 0.05) concurrent with EMG activity from speech production, consistent with speech-induced auditory inhibition. Discrimination conditions were also characterized by α ERS following stimulus offset. Auditory α ERS in all conditions temporally aligned with PMC activity reported in Jenson et al. (2014). These findings are indicative of speech-induced suppression of auditory regions, possibly via efference copy. The presence of the same pattern following stimulus offset in discrimination conditions suggests that sensorimotor contributions following speech perception reflect covert replay, and that covert replay provides one source of the motor activity previously observed in some speech perception tasks. To our knowledge, this is the first time that inhibition of auditory regions by speech has been observed in real-time with the ICA/ERSP technique.

Transcranial alternating current stimulation (tACS) modulates endogenous neural oscillations in healthy human participants by the application of a low-amplitude electrical current with a periodic stimulation waveform. Yet, it is unclear if tACS can modulate and restore neural oscillations that are reduced in patients with psychiatric illnesses such as schizophrenia. Here, we asked if tACS modulates network oscillations in schizophrenia. We performed a randomized, double-blind, sham-controlled clinical trial to contrast tACS with transcranial direct current stimulation (tDCS) and sham stimulation in 22 schizophrenia patients with auditory hallucinations. We used high-density electroencephalography to investigate if a five-day, twice-daily 10Hz-tACS protocol enhances alpha oscillations and modulates network dynamics that are reduced in schizophrenia. We found that 10Hz-tACS enhanced alpha oscillations and modulated functional connectivity in the alpha frequency band. In addition, 10Hz-tACS enhanced the 40Hz auditory steady-state response (ASSR), which is reduced in patients with schizophrenia. Importantly, clinical improvement of auditory hallucinations correlated with enhancement of alpha oscillations and the 40Hz-ASSR. Together, our findings suggest that tACS has potential as a network-level approach to modulate reduced neural oscillations related to clinical symptoms in patients with schizophrenia.

Hearing loss is a major risk factor for tinnitus, hyperacusis, and central auditory processing disorder. Although recent studies indicate that hearing loss causes neuroinflammation in the auditory pathway, the mechanisms underlying hearing loss-related pathologies are still poorly understood. We examined neuroinflammation in the auditory cortex following noise-induced hearing loss (NIHL) and its role in tinnitus in rodent models. Our results indicate that NIHL is associated with elevated expression of proinflammatory cytokines and microglial activation-two defining features of neuroinflammatory responses-in the primary auditory cortex (AI). Genetic knockout of tumor necrosis factor alpha (TNF-α) or pharmacologically blocking TNF-α expression prevented neuroinflammation and ameliorated the behavioral phenotype associated with tinnitus in mice with NIHL. Conversely, infusion of TNF-α into AI resulted in behavioral signs of tinnitus in both wild-type and TNF-α knockout mice with normal hearing. Pharmacological depletion of microglia also prevented tinnitus in mice with NIHL. At the synaptic level, the frequency of miniature excitatory synaptic currents (mEPSCs) increased and that of miniature inhibitory synaptic currents (mIPSCs) decreased in AI pyramidal neurons in animals with NIHL. This excitatory-to-inhibitory synaptic imbalance was completely prevented by pharmacological blockade of TNF-α expression. These results implicate neuroinflammation as a therapeutic target for treating tinnitus and other hearing loss-related disorders.

To protect the audiosensory organ from tissue damage from the immune system, the inner ear is separated from the circulating immune system by the blood-labyrinth barrier, which was previously considered an immune-privileged site. Recent studies have shown that macrophages are distributed in the cochlea, especially in the spiral ligament, spiral ganglion, and stria vascularis; however, the direct pathogen defence mechanism used by audiosensory receptor hair cells (HCs) has remained obscure. Here, we show that HCs are protected from pathogens by surrounding accessory supporting cells (SCs) and greater epithelial ridge (GER or Kölliker’s organ) cells (GERCs). In isolated murine cochlear sensory epithelium, we established Theiler’s murine encephalomyelitis virus, which infected the SCs and GERCs, but very few HCs. The virus-infected SCs produced interferon (IFN)-α/β, and the viruses efficiently infected the HCs in the IFN-α/β receptor-null sensory epithelium. Interestingly, the virus-infected SCs and GERCs expressed macrophage marker proteins and were eliminated from the cell layer by cell detachment. Moreover, lipopolysaccharide induced phagocytosis of the SCs without cell detachment, and the SCs phagocytosed the bacteria. These results reveal that SCs function as macrophage-like cells, protect adjacent HCs from pathogens, and provide a novel anti-infection inner ear immune system.

The neurobiology of Autism Spectrum Disorder (ASD) is hypothetically related to the imbalance between neural excitation (E) and inhibition (I). Different studies have revealed that alpha-band (8–12 Hz) activity in magneto- and electroencephalography (MEG and EEG) may reflect E and I processes and, thus, can be of particular interest in ASD research. Previous findings indicated alterations in event-related and baseline alpha activity in different cortical systems in individuals with ASD, and these abnormalities were associated with core and co-occurring conditions of ASD. However, the knowledge on auditory alpha oscillations in this population is limited. This MEG study investigated stimulus-induced (Event-Related Desynchronization, ERD) and baseline alpha-band activity (both periodic and aperiodic) in the auditory cortex and also the relationships between these neural activities and behavioral measures of children with ASD. Ninety amplitude-modulated tones were presented to two groups of children: 20 children with ASD (5 girls, M age = 10.03, SD  = 1.7) and 20 typically developing controls (9 girls, M age = 9.11, SD  = 1.3). Children with ASD had a bilateral reduction of alpha-band ERD, reduced baseline aperiodic-adjusted alpha power, and flattened aperiodic exponent in comparison to TD children. Moreover, lower raw baseline alpha power and aperiodic offset in the language-dominant left auditory cortex were associated with better language skills of children with ASD measured in formal assessment. The findings highlighted the alterations of E / I balance metrics in response to basic auditory stimuli in children with ASD and also provided evidence for the contribution of low-level processing to language difficulties in ASD.