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Multisensory learning and resulting neural brain plasticity have recently become a topic of renewed interest in human cognitive neuroscience. Music notation reading is an ideal stimulus to study multisensory learning, as it allows studying the integration of visual, auditory and sensorimotor information processing. The present study aimed at answering whether multisensory learning alters uni-sensory structures, interconnections of uni-sensory structures or specific multisensory areas. In a short-term piano training procedure musically naive subjects were trained to play tone sequences from visually presented patterns in a music notation-like system [Auditory-Visual-Somatosensory group (AVS)], while another group received audio-visual training only that involved viewing the patterns and attentively listening to the recordings of the AVS training sessions [Auditory-Visual group (AV)]. Training-related changes in cortical networks were assessed by pre- and post-training magnetoencephalographic (MEG) recordings of an auditory, a visual and an integrated audio-visual mismatch negativity (MMN). The two groups (AVS and AV) were differently affected by the training. The results suggest that multisensory training alters the function of multisensory structures, and not the uni-sensory ones along with their interconnections, and thus provide an answer to an important question presented by cognitive models of multisensory training.

Cortical sensory maps are remodeled during early life to adapt to the surrounding environment. Both sensory and contextual signals are important for induction of this plasticity, but how these signals converge to sculpt developing thalamocortical circuits remains largely unknown. Here we show that layer 1 (L1) of primary auditory cortex (A1) is a key hub where neuromodulatory and topographically organized thalamic inputs meet to tune the cortical layers below. Inhibitory interneurons in L1 send narrowly descending projections to differentially modulate thalamic drive to pyramidal and parvalbumin-expressing (PV) cells in L4, creating brief windows of intracolumnar activation. Silencing of L1 (but not VIP-expressing) cells abolishes map plasticity during the tonotopic critical period. Developmental transitions in nicotinic acetylcholine receptor (nAChR) sensitivity in these cells caused by Lynx1 protein can be overridden to extend critical-period closure. Notably, thalamocortical maps in L1 are themselves stable, and serve as a scaffold for cortical plasticity throughout life.

Deficits in plasticity underlie many severe psychiatric disorders. Transcranial direct current stimulation (tDCS) is a promising method for modulating plasticity. However, given its non-focal nature, there are open questions as to how targeting and outcome specificity can best be achieved. Understanding how tDCS interacts with concurrent brain activity is necessary for the rational advancement of tDCS. In the present study, we use an event-related potential (ERP) paradigm to assess the stimulus-specific effects of tDCS on cortical plasticity. 22 healthy volunteers underwent a blinded, sham-controlled plasticity paradigm in a crossover design. High frequency presentation of auditory stimuli was used to induce potentiation in specific components of the ERP. We investigated whether anodal tDCS targeting the auditory cortex would modulate plasticity induction across time. Two pure tones were used as stimuli, only one of the tones, the target tone, was used for plasticity induction. Plasticity was quantified as change in the mean amplitude of the N100 component relative to baseline. TDCS significantly modulated plasticity in the target tone compared to sham (p ​= ​0.02) but had no effect on the control tone (p ​= ​0.73). This effect was time dependent, with tDCS effects no longer apparent 30 ​min after stimulation. Our results indicate that tDCS can modulate cortical plasticity in the auditory cortex in an activity-dependent manner. These findings bolster the idea that tDCS can be an effective tool to target and modulate plasticity both for research and therapeutic purposes.

Frequency-following responses (FFRs) are neurophonic potentials that provide a window into the encoding of complex sounds (e.g., speech/music), auditory disorders, and neuroplasticity. While the neural origins of the FFR remain debated, renewed controversy has reemerged after demonstration that FFRs recorded via magnetoencephalography (MEG) are dominated by cortical rather than brainstem structures as previously assumed. Here, we recorded high-density (64 ch) FFRs via EEG and applied state-of-the art source imaging techniques to multichannel data (discrete dipole modeling, distributed imaging, independent component analysis, computational simulations). Our data confirm a mixture of generators localized to bilateral auditory nerve (AN), brainstem inferior colliculus (BS), and bilateral primary auditory cortex (PAC). However, frequency-specific scrutiny of source waveforms showed the relative contribution of these nuclei to the aggregate FFR varied across stimulus frequencies. Whereas AN and BS sources produced robust FFRs up to ∼700 Hz, PAC showed weak phase-locking with little FFR energy above the speech fundamental (100 Hz). Notably, CLARA imaging further showed PAC activation was eradicated for FFRs >150 Hz, above which only subcortical sources remained active. Our results show (i) the site of FFR generation varies critically with stimulus frequency; and (ii) opposite the pattern observed in MEG, subcortical structures make the largest contribution to electrically recorded FFRs (AN ≥ BS > PAC). We infer that cortical dominance observed in previous neuromagnetic data is likely due to the bias of MEG to superficial brain tissue, underestimating subcortical structures that drive most of the speech-FFR. Cleanly separating subcortical from cortical FFRs can be achieved by ensuring stimulus frequencies are >150–200 Hz, above the phase-locking limit of cortical neurons.

The auditory frequency-following response (FFR) is a non-invasive index of the fidelity of sound encoding in the brain, and is used to study the integrity, plasticity, and behavioral relevance of the neural encoding of sound. In this Perspective, we review recent evidence suggesting that, in humans, the FFR arises from multiple cortical and subcortical sources, not just subcortically as previously believed, and we illustrate how the FFR to complex sounds can enhance the wider field of auditory neuroscience. Far from being of use only to study basic auditory processes, the FFR is an uncommonly multifaceted response yielding a wealth of information, with much yet to be tapped. The auditory frequency-following response (FFR) indexes the quality of neural sound encoding in the brain. In this Perspective, the authors discuss the potential of the FFR to provide a better understanding of sound encoding in the auditory system and its relationship to behavior.

Musical training is associated with a myriad of neuroplastic changes in the brain, including more robust and efficient neural processing of clean and degraded speech signals at brainstem and cortical levels. These assumptions stem largely from cross-sectional studies between musicians and nonmusicians which cannot address whether training itself is sufficient to induce physiological changes or whether preexisting superiority in auditory function before training predisposes individuals to pursue musical interests and appear to have similar neuroplastic benefits as musicians. Here, we recorded neuroelectric brain activity to clear and noise-degraded speech sounds in individuals without formal music training but who differed in their receptive musical perceptual abilities as assessed objectively via the Profile of Music Perception Skills. We found that listeners with naturally more adept listening skills (“musical sleepers”) had enhanced frequency-following responses to speech that were also more resilient to the detrimental effects of noise, consistent with the increased fidelity of speech encoding and speech-in-noise benefits observed previously in highly trained musicians. Further comparisons between these musical sleepers and actual trained musicians suggested that experience provides an additional boost to the neural encoding and perception of speech. Collectively, our findings suggest that the auditory neuroplasticity of music engagement likely involves a layering of both preexisting (nature) and experience-driven (nurture) factors in complex sound processing. In the absence of formal training, individuals with intrinsically proficient auditory systems can exhibit musician-like auditory function that can be further shaped in an experience-dependent manner.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by complex sensory processing deficits, which continue to elude comprehensive mechanistic understanding. A key unresolved question is how alterations in neural connectivity and communication translate into the behavioral manifestations seen in ASD. Here, we investigate how oligodendrocyte dysfunction alters myelin plasticity and neuronal activity, leading to auditory processing disorder associated with ASD. We focus on the SCN2A gene, an ASD-risk factor, to understand its role in myelination and neural processing within the auditory nervous system. Transcriptional profiling suggests alterations in the expression of myelin-associated genes in Scn2a conditional knockout mice, highlighting the cellular consequences engendered by Scn2a deletion in oligodendrocytes. The results reveal a nuanced interplay between oligodendrocytes and axons, where Scn2a deletion causes alterations in the intricate process of myelination. This disruption instigates changes in axonal properties, presynaptic excitability, and synaptic plasticity at the single cell level. Furthermore, oligodendrocyte-specific Scn2a deletion compromises the integrity of neural circuitry within auditory pathways, leading to auditory hypersensitivity. Our findings reveal a pathway linking myelin deficits to synaptic activity and sensory abnormalities in ASD. Myelin abnormalities in ASD remain poorly understood. Here authors investigate Scn 2a deletion in oligodendrocytes, and report disruptions in myelin, ion channel distribution, and axonal conduction lead to abnormal synaptic plasticity and auditory hypersensitivity.

Infant cries evoke powerful responses in parents 1 – 4 . Whether parental animals are intrinsically sensitive to neonatal vocalizations, or instead learn about vocal cues for parenting responses is unclear. In mice, pup-naive virgin females do not recognize the meaning of pup distress calls, but retrieve isolated pups to the nest after having been co-housed with a mother and litter 5 – 9 . Distress calls are variable, and require co-caring virgin mice to generalize across calls for reliable retrieval 10 , 11 . Here we show that the onset of maternal behaviour in mice results from interactions between intrinsic mechanisms and experience-dependent plasticity in the auditory cortex. In maternal females, calls with inter-syllable intervals (ISIs) from 75 to 375 milliseconds elicited pup retrieval, and cortical responses were generalized across these ISIs. By contrast, naive virgins were neuronally and behaviourally sensitized to the most common (‘prototypical’) ISIs. Inhibitory and excitatory neural responses were initially mismatched in the cortex of naive mice, with untuned inhibition and overly narrow excitation. During co-housing experiments, excitatory responses broadened to represent a wider range of ISIs, whereas inhibitory tuning sharpened to form a perceptual boundary. We presented synthetic calls during co-housing and observed that neurobehavioural responses adjusted to match these statistics, a process that required cortical activity and the hypothalamic oxytocin system. Neuroplastic mechanisms therefore build on an intrinsic sensitivity in the mouse auditory cortex, and enable rapid plasticity for reliable parenting behaviour. The onset of maternal behaviour in mice involves an interaction between intrinsic tuning of auditory cortical neurons and experience-dependent plasticity.

In this article, we introduce a biomimetic audiomorphic device that captures the neurobiological architecture and computational map inside the auditory cortex of barn owl known for its exceptional hunting ability in complete darkness using auditory cues. The device consists of multiple split-gates with nanogaps on a semiconducting MoS 2 channel connected to the source/drain contacts for imitating the spatial map of coincidence detector neurons and tunable RC circuits for imitating the interaural time delay neurons following the Jeffress model of sound localization. Furthermore, we use global back-gating capability to demonstrate neuroplasticity to capture behavioral and/or adaptation related changes in the barn owl. Finally, the virtual source model for current transport is combined with finite element COMSOL multiphysics simulations to explain and project the performance of the biomimetic audiomorphic device. We find that the precision of the biomimetic device can supersede the barn owl by orders of magnitude. Biomimetic audiomorphic functionalities can be implemented in solid-state devices including 2D materials. Here, the authors fabricate a device based on multiple split gates with nano-gaps on a single semiconducting MoS 2 channel that captures the neurobiological architecture and computational map inside the auditory cortex of barn owl.

Practice sharpens our perceptual judgments, a process known as perceptual learning. Although several brain regions and neural mechanisms have been proposed to support perceptual learning, formal tests of causality are lacking. Furthermore, the temporal relationship between neural and behavioral plasticity remains uncertain. To address these issues, we recorded the activity of auditory cortical neurons as gerbils trained on a sound detection task. Training led to improvements in cortical and behavioral sensitivity that were closely matched in terms of magnitude and time course. Surprisingly, the degree of neural improvement was behaviorally gated. During task performance, cortical improvements were large and predicted behavioral outcomes. In contrast, during nontask listening sessions, cortical improvements were weak and uncorrelated with perceptual performance. Targeted reduction of auditory cortical activity during training diminished perceptual learning while leaving psychometric performance largely unaffected. Collectively, our findings suggest that training facilitates perceptual learning by strengthening both bottom-up sensory encoding and top-down modulation of auditory cortex.