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Related Concept Videos

The Vestibular System01:29

The Vestibular System

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The vestibular system is a set of inner ear structures that provide a sense of balance and spatial orientation. This system is comprised of structures within the labyrinth of the inner ear, including the cochlea and two otolith organs—the utricle and saccule. The labyrinth also contains three semicircular canals—superior, posterior, and horizontal—that are oriented on different planes.
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Equilibrium and Balance01:15

Equilibrium and Balance

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The inner ear assumes dual functionalities of auditory perception and equilibrium maintenance. The vestibule is the organ responsible for balance. This organ contains mechanoreceptors, specifically hair cells, endowed with stereocilia, which aid in deciphering information regarding the position and motion of our heads. Two intrinsic components, the utricle and saccule, help perceive head position, while the semicircular canals track head movement. Neurological messages initiated in the...
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Major Somatic Sensory Pathways01:28

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Sensory impulses related to touch, pressure, vibration, and proprioception from various body parts, such as the limbs, trunk, neck, and posterior head, travel to the cerebral cortex through the posterior column-medial lemniscus pathway. The pathway’s name derives from the two white-matter tracts that convey the impulses: the spinal cord's posterior column and the brainstem's medial lemniscus. First-order sensory neurons extend their axons into the spinal cord, forming the...
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Indirect Motor Pathways01:22

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The indirect motor or extrapyramidal pathways originate in the brainstem, the lower portion of the brain that connects it to the spinal cord. They consist of several distinct tracts, each with specialized functions. The four main tracts of the indirect motor pathways are the vestibulospinal tract, the reticulospinal tract, the tectospinal tract, and the rubrospinal tract.
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Vision01:24

Vision

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Vision is the result of light being detected and transduced into neural signals by the retina of the eye. This information is then further analyzed and interpreted by the brain. First, light enters the front of the eye and is focused by the cornea and lens onto the retina—a thin sheet of neural tissue lining the back of the eye. Because of refraction through the convex lens of the eye, images are projected onto the retina upside-down and reversed.
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Related Experiment Video

Updated: Jan 9, 2026

Using Eye-tracking to Assess the Relative Importance of Visual and Vestibular Input to Subcortical Motion Processing in the Roll Plane
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Using Eye-tracking to Assess the Relative Importance of Visual and Vestibular Input to Subcortical Motion Processing in the Roll Plane

Published on: August 22, 2025

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Unilateral peripheral vestibular dysfunction disrupts motion-evoked neuronal responses in primary visual cortex.

Jiawei Feng1, Yumeng Jiang1, Pengjun Wang1

  • 1Department of Otorhinolaryngology Head & Neck Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200233, China.

Neurobiology of Disease
|December 5, 2025
PubMed
Summary

Peripheral vestibular damage disrupts visual processing in the brain, causing dizziness. Compensatory neural activity in the vestibular system interferes with how the primary visual cortex (V1) responds to motion, leading to these symptoms.

Keywords:
CochleaeHearingTwo-photon microscopyVestibular dysfunction

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Area of Science:

  • Neuroscience
  • Vestibular System Research
  • Visual Cortex Function

Background:

  • Acute unilateral peripheral vestibular destruction (AUPVD) causes dizziness with visual and motion disturbances.
  • The vestibular nuclei integrate auditory and visual inputs, crucial for balance and gaze.
  • The influence of vestibular activity on the primary visual cortex (V1) is not fully understood.

Purpose of the Study:

  • To investigate the impact of vestibular nuclei activity on V1 neuronal responses to visual stimuli.
  • To elucidate the mechanisms by which vestibular damage affects visual processing in V1.
  • To determine the role of vestibular inhibitory neurons in V1 dysfunction following vestibular lesions.

Main Methods:

  • Chronic two-photon microscopy in awake AUPVD mice to observe V1 neuronal activity.
  • Assessment of V1 neuronal responses to both static and motion visual stimuli.
  • Pharmacological and chemogenetic manipulation of GABAergic signaling in the vestibular nuclei of healthy mice.

Main Results:

  • V1 neurons in AUPVD mice showed impaired responses to motion stimuli but normal responses to static visual inputs.
  • Aberrant activity in vestibular inhibitory neurons, induced pharmacologically or chemogenetically, disrupted V1 neuronal processing in healthy mice.
  • Compensatory firing patterns in vestibular inhibitory neurons were identified as a key factor.

Conclusions:

  • Vestibular activity significantly influences V1 processing of motion-related visual stimuli.
  • Disrupted vestibular inhibitory neuron function following peripheral vestibular damage impairs V1 responses to motion.
  • These V1 processing deficits contribute to the dizziness experienced after vestibular damage.