Explore the vast range of titles available.

Spontaneous activity in the developing auditory system is required for neuronal survival as well as the refinement and maintenance of tonotopic maps in the brain. However, the mechanisms responsible for initiating auditory nerve firing in the absence of sound have not been determined. Here we show that supporting cells in the developing rat cochlea spontaneously release ATP, which causes nearby inner hair cells to depolarize and release glutamate, triggering discrete bursts of action potentials in primary auditory neurons. This endogenous, ATP-mediated signalling synchronizes the output of neighbouring inner hair cells, which may help refine tonotopic maps in the brain. Spontaneous ATP-dependent signalling rapidly subsides after the onset of hearing, thereby preventing this experience-independent activity from interfering with accurate encoding of sound. These data indicate that supporting cells in the organ of Corti initiate electrical activity in auditory nerves before hearing, pointing to an essential role for peripheral, non-sensory cells in the development of central auditory pathways.

Auditory perception is established through experience‐dependent stimuli exposure during sensitive developmental periods; however, little is known regarding the structural development of the central auditory pathway in humans. The present study characterized the regional developmental trajectories of the ascending auditory pathway from the brainstem to the auditory cortex from infancy through adolescence using a novel diffusion MRI‐based tractography approach and along‐tract analyses. We used diffusion tensor imaging (DTI) and neurite orientation dispersion and density imaging (NODDI) to quantify the magnitude and timing of auditory pathway microstructural maturation. We found spatially varying patterns of white matter maturation along the length of the tract, with inferior brainstem regions developing earlier than thalamocortical projections and left hemisphere tracts developing earlier than the right. These results help to characterize the processes that give rise to functional auditory processing and may provide a baseline for detecting abnormal development. The present study characterizes the microstructural maturation of the auditory pathway from infancy through adolescence using diffusion MRI models. Using NODDI and DTI, we demonstrate auditory pathway maturation is heterogeneous, where brainstem structures mature prior to subcortical white matter.

Key Points An auditory object is a perceptual construct, corresponding to the sound that can be assigned to a particular acoustic source. An auditory object spans acoustic events that unfold over time, and a sequence of objects forms a 'stream': for example, when a person is walking, the sound of each step is a unique auditory object but the temporal sequence of footsteps is linked together to form a stream. An auditory object is constructed from the spectrotemporal regularities in the acoustic environment. More specifically, an auditory stimulus comes into our awareness as a sound as a result of the simultaneous and sequential principles that group the acoustic features of the auditory stimulus into stable spectrotemporal entities. Auditory-object processing occurs in the cortex. In particular, the ventral auditory pathway mediates the computations underlying a listener's ability to perceive a sound (auditory object), whereas object-related information that is found in the dorsal pathway is used in the pursuit of audiomotor behaviours. Neural correlates of the perception of an auditory object are found in the auditory cortex. Whereas some studies indicate that the ventral pathway contains brain regions specialized for auditory-object processing, auditory perception is most likely to be mediated by a broad network of brain areas in this pathway. A hallmark of auditory-object processing is that it can be influenced by attention and that attention can act on the object itself and not the lower-level spectrotemporal details of the auditory stimulus. Both single-unit and functional imaging studies demonstrate the effects of attention on the representation of auditory objects in the auditory cortex. In order to make sense of the multitude of acoustic stimuli that surround us in our daily lives, the auditory system needs to be able to assign different sounds to specific sources within the 'auditory scene'. Bizley and Cohen describe how auditory information processing in the cortex categorizes and groups different sounds into 'auditory objects'. The fundamental perceptual unit in hearing is the 'auditory object'. Similar to visual objects, auditory objects are the computational result of the auditory system's capacity to detect, extract, segregate and group spectrotemporal regularities in the acoustic environment; the multitude of acoustic stimuli around us together form the auditory scene. However, unlike the visual scene, resolving the component objects within the auditory scene crucially depends on their temporal structure. Neural correlates of auditory objects are found throughout the auditory system. However, neural responses do not become correlated with a listener's perceptual reports until the level of the cortex. The roles of different neural structures and the contribution of different cognitive states to the perception of auditory objects are not yet fully understood.

Key Points Tinnitus is prevalent in up to 15% of the world population Tinnitus is linked to hearing loss: loss of input from the cochlea to central auditory pathways triggers plastic neural changes that result in increased spontaneous activity and synchrony in affected regions Neurons in nonauditory regions are also affected by tinnitus Although tinnitus is often linked to noise exposure, tinnitus does not always occur after noise damage in humans or animal models An understanding of the neural mechanisms of tinnitus is essential for developing effective treatments Tinnitus, prevalent in up to 15% of the world population, is typically linked to noise-associated hearing loss, but the relationship between noise exposure and tinnitus is not straightforward: not all humans or model animals develop tinnitus after noise-associated cochlear damage, and the mechanisms involved in tinnitus involve central auditory system and nonauditory brain areas. This Review provides an overview of current understanding of neural mechanisms of tinnitus, which is essential for developing effective treatments for this disorder. Tinnitus is a phantom auditory sensation that reduces quality of life for millions of people worldwide, and for which there is no medical cure. Most cases of tinnitus are associated with hearing loss caused by ageing or noise exposure. Exposure to loud recreational sound is common among the young, and this group are at increasing risk of developing tinnitus. Head or neck injuries can also trigger the development of tinnitus, as altered somatosensory input can affect auditory pathways and lead to tinnitus or modulate its intensity. Emotional and attentional state could be involved in the development and maintenance of tinnitus via top-down mechanisms. Thus, military personnel in combat are particularly at risk owing to combined risk factors (hearing loss, somatosensory system disturbances and emotional stress). Animal model studies have identified tinnitus-associated neural changes that commence at the cochlear nucleus and extend to the auditory cortex and other brain regions. Maladaptive neural plasticity seems to underlie these changes: it results in increased spontaneous firing rates and synchrony among neurons in central auditory structures, possibly generating the phantom percept. This Review highlights the links between animal and human studies, and discusses several therapeutic approaches that have been developed to target the neuroplastic changes underlying tinnitus.

Humans and other animals use spatial hearing to rapidly localize events in the environment. However, neural encoding of sound location is a complex process involving the computation and integration of multiple spatial cues that are not represented directly in the sensory organ (the cochlea). Our understanding of these mechanisms has increased enormously in the past few years. Current research is focused on the contribution of animal models for understanding human spatial audition, the effects of behavioural demands on neural sound location encoding, the emergence of a cue-independent location representation in the auditory cortex, and the relationship between single-source and concurrent location encoding in complex auditory scenes. Furthermore, computational modelling seeks to unravel how neural representations of sound source locations are derived from the complex binaural waveforms of real-life sounds. In this article, we review and integrate the latest insights from neurophysiological, neuroimaging and computational modelling studies of mammalian spatial hearing. We propose that the cortical representation of sound location emerges from recurrent processing taking place in a dynamic, adaptive network of early (primary) and higher-order (posterior–dorsal and dorsolateral prefrontal) auditory regions. This cortical network accommodates changing behavioural requirements and is especially relevant for processing the location of real-life, complex sounds and complex auditory scenes.

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.

Key Points Individuals with schizophrenia show deficits in auditory sensory processing that represent a core feature of the disorder. At the behavioural level, patients are impaired in the ability to match tones or to detect the 'musicality' of speech (prosody). Deficits in the ability to correctly detect non-verbal elements of speech (for example, emotion and attitude) contributes greatly to the social disability associated with schizophrenia. Impaired auditory processing also leads to degeneration of phonological reading ability that first becomes manifest during the early stages of the disorder and which contributes to educational and occupational impairment. At the neurophysiological level, deficits are reflected in impaired generation of mismatch negativity and other event-related potentials that are generated primarily within the auditory sensory cortex. These deficits, in turn, are linked to dysfunction in NMDA receptor-mediated neurotransmission. The deficits in auditory processing are mirrored by objective histological changes observed in the post-mortem auditory cortex in schizophrenia. Histological changes show reductions in spine density and alterations in glutamatergic transmission, which is consistent with the pattern of functional impairment. Overall, these findings encourage the use of auditory neurophysiological measures for cross-species aetiological and pharmacological research into schizophrenia. Schizophrenia is characterized by various neurocognitive deficits, including impairments in auditory function. In this Review, Javitt and Sweet examine the behavioural, neurophysiological and structural evidence for auditory cortical dysfunction in this disorder and explore some of the possible underlying mechanisms. Schizophrenia is a complex neuropsychiatric disorder that is associated with persistent psychosocial disability in affected individuals. Although studies of schizophrenia have traditionally focused on deficits in higher-order processes such as working memory and executive function, there is an increasing realization that, in this disorder, deficits can be found throughout the cortex and are manifest even at the level of early sensory processing. These deficits are highly amenable to translational investigation and represent potential novel targets for clinical intervention. Deficits, moreover, have been linked to specific structural abnormalities in post-mortem auditory cortex tissue from individuals with schizophrenia, providing unique insights into underlying pathophysiological mechanisms.

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.

There are functional and anatomical distinctions between the neural systems involved in the recognition of sounds in the environment and those involved in the sensorimotor guidance of sound production and the spatial processing of sound. Evidence for the separation of these processes has historically come from disparate literatures on the perception and production of speech, music and other sounds. More recent evidence indicates that there are computational distinctions between the rostral and caudal primate auditory cortex that may underlie functional differences in auditory processing. These functional differences may originate from differences in the response times and temporal profiles of neurons in the rostral and caudal auditory cortex, suggesting that computational accounts of primate auditory pathways should focus on the implications of these temporal response differences.How is the processing of auditory information by the cortex organized? Scott and colleagues describe differences in the connectivity and properties of the rostral and caudal auditory cortex and propose links to the functional specializations of the rostral and caudal auditory streams.

Purpose Objective information about the central auditory pathways in vestibular schwannoma can guide strategies for hearing rehabilitation and prognostication. This study aims to generate this information using diffusion tensor imaging (DTI). Methods This is a prospective observational single center study including 35 patients with vestibular schwannoma and 40 controls. Subjects underwent 64 direction multi-shell DTI which was processed to yield scalar parameters [Fractional Anisotropy (FA) and Apparent Diffusion Coefficient (ADC)] and probabilistic fiber tracking parameters. Results FA values were found to be significantly reduced at bilateral medial geniculate bodies and contralateral inferior colliculus ( P  < 0.001). In contrast, FA values were significantly increased at bilateral Heschl’s gyrus ( P  < 0.001). This was further validated by a progressive increase in FA values at bilateral Heschl’s gyri with increasing tumor size. Contralateral inferior colliculus showed a marginal increase in FA value ( P  = 0.006) and a marginal decrease in ADC value ( P  = 0.045) in patients with nonfunctional hearing as compared to patients with functional hearing. Rest of the DTI parameters were comparable across patient groups based on duration of hearing loss, hearing function, tumor location and tumor size. FA values along the tracts and the tract volumes were reduced significantly on both the sides ( P  < 0.001). Conclusion Vestibular schwannoma induces degenerative changes in subcortical auditory pathways bilaterally; bilateral medial geniculate bodies and contralateral inferior colliculi being the epicenters of these changes. Primary auditory cortex attempts to reorganize and adjust to the loss of these subcortical inputs.