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URMC / Labs / Newlands Lab / Projects / Peripheral Vestibular Lesions and Vestibular System Plasticity

Peripheral Vestibular Lesions and Vestibular System Plasticity

The vestibular end organs in the inner ear, three pairs of semicircular canals and two pairs of otolith organs (the utricle and saccule), provide information of how the head rotates in three-dimensional space and how the body translates in space and posts relatively to gravity respectively. Vestibular nuclei neurons receive signals from these sensors as well as from convergent information of visual, proprioceptive systems, and information concerning oculomotor-related activity from the pre-motor brainstem and cerebellar structures. Loss of unilateral labyrinthine input to the vestibular nuclei creates a series of behavior problems such as vertigo, nausea and vomiting, eye nystagmus movement, etc. Such symptoms will eventually disappear which is attributed to the function of vestibular compensation. However, the central mechanisms of the vestibular compensation after lesion remain unclear. From the neural responses in the brainstem, mainly from vestibular nuclei, we focus on understanding the time course and dynamic properties of compensation mechanism after the lesion through behavior and neural response analysis experiments.

neuron signal plot

A Vestibular-Only neuron is a type of
neuron sensitive to the head movement only.

neuron signal plot

A Position-Vestibular-Pause neuron is
a type of neuron sensitive to both eye
and head movements in opposite (complementary)
directions, but pause during saccadic movements.

neuron signal plot

A Eye-Head-Velocity neuron is a type of
neuron sensitive to both eye and head movements
but in the same directions, such
that two signals cancel each other during head
movement while stabilizing an earth-fixed target.

By rotation and translation of the subject while recording neural responses from vestibular nuclei and adjacent areas, we can see if the lesion changes any dynamic character of neural responses and their possible recover course in neurons such as broadly-tuned neurons which have both spatial and temporal tuning characters. We can examine how small the head perturbation could effectively activate the neural responses to keep vision clear through eye movement reflex or maintain body balance. Sensory neurons are known to adapt to differing levels of stimulation, resulting in extended dynamic ranges of their responses. This process, known as gain control, sensory adaptation or adaptive rescaling, has been demonstrated in several sensory systems and can occur rapidly. By analyzing the neural responses with rotating subjects from low velocity transition to high velocity or vice verse, we can tell if the secondary vestibular neurons have such adaptive ability and its time course.

Active vs. Passive Head Movement

It is important to emphasize that all above experiments are performed under the head-restrained conditions. Until recently, the vestibular system had been exclusively studied in such a head-restrained condition. As a result, neural processes in the vestibular nuclei are limited to respond to the ex-afferent inputs from the vestibular end organs. With active head movement, the brain needs to differentiate sensory signals from the vestibular end organs generated by the self motion or by the environment movement, which could make the neural process more complicated. Recently, literatures have demonstrated the dramatic differences of neural responses in the vestibular nuclei between active and passive movements. Vestibular compensation following peripheral vestibular lesion appears more complete during active head movement than during passive head movements. By recording neural responses in conditions of passive whole body or head only motion and also self active head motion, we are interested in studying why the active movements is better than passive movement in the recovery and the potential recovery mechanism in the active conditions would be benefit to the medical intervention.

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