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Related Concept Videos

Hearing01:31

Hearing

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When we hear a sound, our nervous system is detecting sound waves—pressure waves of mechanical energy traveling through a medium. The frequency of the wave is perceived as pitch, while the amplitude is perceived as loudness.
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Auditory Pathway01:15

Auditory Pathway

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Auditory pathways constitute the complex neural circuits responsible for transmitting and interpreting auditory information from the peripheral auditory system to the brain. Sound waves are initially captured by the outer ear, funneled through the ear canal, and reach the tympanic membrane (eardrum). These vibrations are transmitted via the middle ear's ossicles to the inner ear's cochlea.
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The Cochlea01:13

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The cochlea is a coiled structure in the inner ear that contains hair cells—the sensory receptors of the auditory system. Sound waves are transmitted to the cochlea by small bones attached to the eardrum called the ossicles, which vibrate the oval window that leads to the inner ear. This causes fluid in the chambers of the cochlea to move, vibrating the basilar membrane.
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Hair Cells01:22

Hair Cells

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Hair cells are the sensory receptors of the auditory system—they transduce mechanical sound waves into electrical energy that the nervous system can understand. Hair cells are located in the organ of Corti within the cochlea of the inner ear, between the basilar and tectorial membranes. The actual sensory receptors are called inner hair cells. The outer hair cells serve other functions, such as sound amplification in the cochlea, and are not discussed in detail here.
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Perceiving Loudness, Pitch, and Location01:21

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The human brain perceives pitch through two primary mechanisms reflected in place theory and frequency theory. Each mechanism describes how sound waves are interpreted as specific pitches by the brain, offering insights into the intricate processes of auditory perception.
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Anatomy of the Ear01:16

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Auditory sensation, commonly called hearing, involves the transformation of sonic waves into neural impulses facilitated by the structures of the auditory organ. The prominent, flesh-like structure on the side of the head, called the auricle, directs sound waves towards the auditory canal. The auricle is often mislabeled as the pinna, a term more aligned with mobile structures like a feline's external ear. The auditory canal penetrates the cranium via the external auditory meatus of the...
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Related Experiment Video

Updated: Mar 15, 2026

Cochlear Implant Surgery and Electrically-evoked Auditory Brainstem Response Recordings in C57BL/6 Mice
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Persistent Thalamic Sound Processing Despite Profound Cochlear Denervation.

Anna R Chambers1, Juan J Salazar2, Daniel B Polley3

  • 1Eaton-Peabody Laboratories, Massachusetts Eye and Ear Infirmary Boston, MA, USA.

Frontiers in Neural Circuits
|September 16, 2016
PubMed
Summary
This summary is machine-generated.

Central gain partially restores auditory processing in the thalamus after severe hearing loss, but less effectively than in the cortex or midbrain. This suggests hierarchical differences in brain plasticity following auditory neuropathy.

Keywords:
cochlear neuropathycompensatory plasticityhearing losshomeostatic plasticitymedial geniculate body

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Stereotactically-guided Ablation of the Rat Auditory Cortex, and Localization of the Lesion in the Brain
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Area of Science:

  • Neuroscience
  • Auditory Neuroscience
  • Sensory Plasticity

Background:

  • Neurons can compensate for lost sensory input via homeostatic plasticity, increasing gain on weak signals.
  • Profound unilateral auditory neuropathy (>95% synapse loss) can be compensated by central gain, restoring cortical processing and sound perception.
  • Auditory cortex (ACtx) and inferior colliculus (IC) show recovery in auditory neuropathy models, but the auditory thalamus's plasticity remains less understood.

Purpose of the Study:

  • To investigate compensatory plasticity in the auditory thalamus (medial geniculate body, MGB) following profound cochlear neuropathy.
  • To compare the extent of central gain-mediated plasticity in the MGB to that previously observed in the ACtx and IC.

Main Methods:

  • Induced profound unilateral cochlear neuropathy in adult mice using ouabain, eliminating the auditory brainstem response (ABR).
  • Recorded sound-evoked activity in the contralateral medial geniculate body (MGB) of awake, ouabain-treated and control mice.
  • Analyzed MGB unit responses to pure tones, broadband pulse trains, and speech tokens to assess sound processing capabilities.

Main Results:

  • Despite absent ABR, robust sound-evoked activity persisted in a subset of MGB units in ouabain-treated mice.
  • MGB units could decode moderate and high-intensity sounds comparably to controls, but low-intensity sound decoding was impaired.
  • Receptive field quality and synchronization precision were reduced, and decoding of temporal modulations and speech was significantly impaired.

Conclusions:

  • Persistent auditory processing in the MGB, despite absent ABR, is likely mediated by increased central gain.
  • Compensatory plasticity in the auditory thalamus is less robust than in the auditory cortex or midbrain.
  • Hierarchical differences in compensatory plasticity may stem from distinct GABAergic circuit organizations in the MGB compared to the ACtx or IC.