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The inferior colliculus (IC) is a unique structure in the auditory system, located between the primary auditory nuclei of the brainstem and the thalamus. The existence of the complex neural circuits in the auditory brainstem and midbrain, lacking in other sensory systems, has motivated an outpouring of research on the circuitry and physiological properties of the IC. IC neurons receive ascending inputs from over 20 separate sources in the brainstem as well as a dense collection of descending connections from the cortex. It is richly connected to both the left and right ears through these circuits and a major theme in research on the IC has been its role in binaural interactions. A second theme is the role of descending circuits in modulating responses to sound in the IC. A third theme is understanding the sound processing that occurs at the level of the IC, essentially how the representation of sound in the IC differs from that in the two auditory nerves. The representation of sound in the IC is an intermediate step in the development of the cortical representation as well as in the development of many perceptual features of sounds. These characteristics have been documented for a number of computations, including sound localization, masking properties, robustness of the representation, and responses to temporal and spectral properties of sounds. This Research Topic aims to discuss a wide range of aspects of the structure and function of the IC in a way that will facilitate future research.

Inferior colliculus. --- Brain. --- ion channel models --- inferior colliculus --- sona --- representation of sound --- internal circuitry --- Neural Pathways --- inhibitory circuits

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The inferior colliculus (IC) is a unique structure in the auditory system, located between the primary auditory nuclei of the brainstem and the thalamus. The existence of the complex neural circuits in the auditory brainstem and midbrain, lacking in other sensory systems, has motivated an outpouring of research on the circuitry and physiological properties of the IC. IC neurons receive ascending inputs from over 20 separate sources in the brainstem as well as a dense collection of descending connections from the cortex. It is richly connected to both the left and right ears through these circuits and a major theme in research on the IC has been its role in binaural interactions. A second theme is the role of descending circuits in modulating responses to sound in the IC. A third theme is understanding the sound processing that occurs at the level of the IC, essentially how the representation of sound in the IC differs from that in the two auditory nerves. The representation of sound in the IC is an intermediate step in the development of the cortical representation as well as in the development of many perceptual features of sounds. These characteristics have been documented for a number of computations, including sound localization, masking properties, robustness of the representation, and responses to temporal and spectral properties of sounds. This Research Topic aims to discuss a wide range of aspects of the structure and function of the IC in a way that will facilitate future research.

Inferior colliculus. --- Brain. --- ion channel models --- inferior colliculus --- sona --- representation of sound --- internal circuitry --- Neural Pathways --- inhibitory circuits --- ion channel models --- inferior colliculus --- sona --- representation of sound --- internal circuitry --- Neural Pathways --- inhibitory circuits

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The sense of hearing is vulnerable to environmental challenges, such as exposure to noise. More than 1.5 billion people experience some decline in hearing ability during their lifetime, of whom at least 430 million will be affected by disabling hearing loss. If not identified and addressed in a timely way, hearing loss can severely reduce the quality of life at various stages. Some causes of hearing loss can be prevented, for example from occupational or leisure noise. The World Health Organization estimates that more than 1 billion young people put themselves at risk of permanent hearing loss by listening to loud music over long periods of time. Mitigating such risks through public health action is essential to reduce the impact of hearing loss in the community. The etiology of sensorineural hearing loss is complex and multifactorial, arising from congenital and acquired causes. This book highlights the diverse range of approaches to sensorineural hearing loss, from designing new animal models of age-related hearing loss, to the use of microRNAs as biomarkers of cochlear injury and drug repurposing for the therapy of age-related and noise-induced hearing loss. Further investigation into the underlying molecular mechanisms of sensorineural hearing loss and the integration of the novel drug, cell, and gene therapy strategies into controlled clinical studies will permit significant advances in a field where there are currently many unmet needs.

Medicine --- brain-derived neurotrophic factor --- TrkB --- inner ear --- development --- zebrafish --- mitochondria dysfunction --- reactive oxygen species --- hypoxic --- d-galactose --- high-fat diet --- aging --- hearing loss --- astrocytes --- auditory brainstem --- lateral superior olive --- gap junctions --- voltage-activated calcium channel 1.3 --- otoferlin --- spontaneous activity --- deafness --- circadian dysregulation --- clock genes --- noise-induced hearing loss --- sensory hair cells --- synaptic ribbons --- sensorineural hearing loss --- hyperbaric oxygenation --- adjunctive therapy --- microRNAs --- cochlear nucleus --- inferior colliculus --- neuroplasticity --- noise-induced cochlear injury --- cochlear rescue --- otoprotection --- adenosine A1 receptor --- regulator of G protein signalling 4 --- CCG-4986 --- intratympanic drug delivery --- potassium voltage-gated channel subfamily q member 4 --- potassium --- nonsyndromic hearing loss --- KCNQ4 activator --- age-related hearing loss --- selegiline --- chronic oral treatment --- hearing protection --- mouse model --- brain-derived neurotrophic factor --- TrkB --- inner ear --- development --- zebrafish --- mitochondria dysfunction --- reactive oxygen species --- hypoxic --- d-galactose --- high-fat diet --- aging --- hearing loss --- astrocytes --- auditory brainstem --- lateral superior olive --- gap junctions --- voltage-activated calcium channel 1.3 --- otoferlin --- spontaneous activity --- deafness --- circadian dysregulation --- clock genes --- noise-induced hearing loss --- sensory hair cells --- synaptic ribbons --- sensorineural hearing loss --- hyperbaric oxygenation --- adjunctive therapy --- microRNAs --- cochlear nucleus --- inferior colliculus --- neuroplasticity --- noise-induced cochlear injury --- cochlear rescue --- otoprotection --- adenosine A1 receptor --- regulator of G protein signalling 4 --- CCG-4986 --- intratympanic drug delivery --- potassium voltage-gated channel subfamily q member 4 --- potassium --- nonsyndromic hearing loss --- KCNQ4 activator --- age-related hearing loss --- selegiline --- chronic oral treatment --- hearing protection --- mouse model

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• Reference Manager
• EndNote
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The sense of hearing is vulnerable to environmental challenges, such as exposure to noise. More than 1.5 billion people experience some decline in hearing ability during their lifetime, of whom at least 430 million will be affected by disabling hearing loss. If not identified and addressed in a timely way, hearing loss can severely reduce the quality of life at various stages. Some causes of hearing loss can be prevented, for example from occupational or leisure noise. The World Health Organization estimates that more than 1 billion young people put themselves at risk of permanent hearing loss by listening to loud music over long periods of time. Mitigating such risks through public health action is essential to reduce the impact of hearing loss in the community. The etiology of sensorineural hearing loss is complex and multifactorial, arising from congenital and acquired causes. This book highlights the diverse range of approaches to sensorineural hearing loss, from designing new animal models of age-related hearing loss, to the use of microRNAs as biomarkers of cochlear injury and drug repurposing for the therapy of age-related and noise-induced hearing loss. Further investigation into the underlying molecular mechanisms of sensorineural hearing loss and the integration of the novel drug, cell, and gene therapy strategies into controlled clinical studies will permit significant advances in a field where there are currently many unmet needs.

brain-derived neurotrophic factor --- TrkB --- inner ear --- development --- zebrafish --- mitochondria dysfunction --- reactive oxygen species --- hypoxic --- d-galactose --- high-fat diet --- aging --- hearing loss --- astrocytes --- auditory brainstem --- lateral superior olive --- gap junctions --- voltage-activated calcium channel 1.3 --- otoferlin --- spontaneous activity --- deafness --- circadian dysregulation --- clock genes --- noise-induced hearing loss --- sensory hair cells --- synaptic ribbons --- sensorineural hearing loss --- hyperbaric oxygenation --- adjunctive therapy --- microRNAs --- cochlear nucleus --- inferior colliculus --- neuroplasticity --- noise-induced cochlear injury --- cochlear rescue --- otoprotection --- adenosine A1 receptor --- regulator of G protein signalling 4 --- CCG-4986 --- intratympanic drug delivery --- potassium voltage-gated channel subfamily q member 4 --- potassium --- nonsyndromic hearing loss --- KCNQ4 activator --- age-related hearing loss --- selegiline --- chronic oral treatment --- hearing protection --- mouse model --- n/a