Orientation adaptation of eye movement–related vestibular neurons due to prolonged head tilt

Kolesnikova, Olga V.; Raphan, Theodore; Cohen, Bernard; Yakushin, Sergei B.

doi:10.1111/j.1749-6632.2011.06176.x

Cited by 5 publications

(17 citation statements)

References 21 publications

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“…One of the most important discoveries that could provide a basis for modeling amplitude-dependent learning is orientation adaptation that is present in vestibular only (VO) and position-vestibular-pause (PVP) neurons (Eron et al 2008; Kolesnikova et al 2011b). Such orientation adaptation reconfigures the orientation of a specific group of vestibular cells, but central otolith-only units maintain their spatial orientation (Eron et al 2009).…”

Section: Resultsmentioning

confidence: 99%

“…We have hypothesized that the otolith–canal convergent neurons in the central vestibular system regulate the gravity-dependent aVOR gain adaptation (Kolesnikova et al 2011a). Their functions are simulated as polarization vectors that have various orientations re gravity in the three canal planes.…”

Section: Resultsmentioning

confidence: 99%

“…For data-model comparison, we utilized a reduced case of the analysis of variance (F statistic). These methodologies are completely described in previous publications (Yakushin et al 1995; Kolesnikova et al 2011b). …”

Section: Experimental Methodsmentioning

confidence: 99%

“…Another explanation could be related to our recent findings that there are classes of otolith–canal convergent neurons, which adapt their polarization vectors toward the direction of gravity during side positions (Eron et al 2008; Kolesnikova et al 2011b) and other classes that do not (Eron et al 2009). These neurons could provide a head fixed reference for determining the context for implementation of a specific gain.…”

Section: Introductionmentioning

confidence: 95%

“…We previously demonstrated that the amount of gravity-dependent gain changes is similar for yaw and pitch aVOR, regardless of whether gain was increased or decreased. Thus, this study was restricted to yaw aVOR gain decrease in side-down positions and forms the basis for modeling the behavior of neurons that adapt their orientation (Eron et al 2008; Kolesnikova et al 2011b) and how they contribute to localized gravity-dependent adaptation.…”

Section: Introductionmentioning

confidence: 99%

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Modeling spatial tuning of adaptation of the angular vestibulo-ocular reflex

2012

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Gain adaptation of the yaw angular vestibular ocular reflex (aVOR) induced in side-down positions has gravity-independent (global) and -dependent (localized) components. When the head oscillation angles are small during adaptation, localized gain changes are maximal in the approximate position of adaptation. Concurrently, polarization vectors of canal–otolith vestibular neurons adapt their orientations during these small-angle adaptation paradigms. Whether there is orientation adaptation with large amplitude head oscillations, when the head is not localized to a specific position, is unknown. Yaw aVOR gains were decreased by oscillating monkeys about a yaw axis in a side-down position in a subject–stationary visual surround for 2 h. Amplitudes of head oscillation ranged from 15° to 180°. The yaw aVOR gain was tested in darkness at 0.5 Hz, with small angles of oscillation (±15°) while upright and in tilted positions. The peak value of the gain change was highly tuned for small angular oscillations during adaptation and significantly broadened with larger oscillation angles during adaptation. When the orientation of the polarization vectors associated with the gravity-dependent component of the neural network model was adapted toward the direction of gravity, it predicted the localized learning for small angles and the broadening when the orientation adaptation was diminished. The model-based analysis suggests that the otolith orientation adaptation plays an important role in the localized behavior of aVOR as a function of gravity and in regulating the relationship between global and localized adaptation.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Experimental Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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Modeling spatial tuning of adaptation of the angular vestibulo-ocular reflex

2012

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The neural basis of motion sickness

Cohen

Dai

Yakushin

et al. 2019

Journal of Neurophysiology

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Although motion of the head and body has been suspected or known as the provocative cause for the production of motion sickness for centuries, it is only within the last 20 yr that the source of the signal generating motion sickness and its neural basis has been firmly established. Here, we briefly review the source of the conflicts that cause the body to generate the autonomic signs and symptoms that constitute motion sickness and provide a summary of the experimental data that have led to an understanding of how motion sickness is generated and can be controlled. Activity and structures that produce motion sickness include vestibular input through the semicircular canals, the otolith organs, and the velocity storage integrator in the vestibular nuclei. Velocity storage is produced through activity of vestibular-only (VO) neurons under control of neural structures in the nodulus of the vestibulo-cerebellum. Separate groups of nodular neurons sense orientation to gravity, roll/tilt, and translation, which provide strong inhibitory control of the VO neurons. Additionally, there are acetylcholinergic projections from the nodulus to the stomach, which along with other serotonergic inputs from the vestibular nuclei, could induce nausea and vomiting. Major inhibition is produced by the GABAB receptors, which modulate and suppress activity in the velocity storage integrator. Ingestion of the GABAB agonist baclofen causes suppression of motion sickness. Hopefully, a better understanding of the source of sensory conflict will lead to better ways to avoid and treat the autonomic signs and symptoms that constitute the syndrome.

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Coding of Velocity Storage in the Vestibular Nuclei

2017

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Semicircular canal afferents sense angular acceleration and output angular velocity with a short time constant of ≈4.5 s. This output is prolonged by a central integrative network, velocity storage that lengthens the time constants of eye velocity. This mechanism utilizes canal, otolith, and visual (optokinetic) information to align the axis of eye velocity toward the spatial vertical when head orientation is off-vertical axis. Previous studies indicated that vestibular-only (VO) and vestibular-pause-saccade (VPS) neurons located in the medial and superior vestibular nucleus could code all aspects of velocity storage. A recently developed technique enabled prolonged recording while animals were rotated and received optokinetic stimulation about a spatial vertical axis while upright, side-down, prone, and supine. Firing rates of 33 VO and 8 VPS neurons were studied in alert cynomolgus monkeys. Majority VO neurons were closely correlated with the horizontal component of velocity storage in head coordinates, regardless of head orientation in space. Approximately, half of all tested neurons (46%) code horizontal component of velocity in head coordinates, while the other half (54%) changed their firing rates as the head was oriented relative to the spatial vertical, coding the horizontal component of eye velocity in spatial coordinates. Some VO neurons only coded the cross-coupled pitch or roll components that move the axis of eye rotation toward the spatial vertical. Sixty-five percent of these VO and VPS neurons were more sensitive to rotation in one direction (predominantly contralateral), providing directional orientation for the subset of VO neurons on either side of the brainstem. This indicates that the three-dimensional velocity storage integrator is composed of directional subsets of neurons that are likely to be the bases for the spatial characteristics of velocity storage. Most VPS neurons ceased firing during drowsiness, but the firing rates of VO neurons were unaffected by states of alertness and declined with the time constant of velocity storage. Thus, the VO neurons are the prime components of the mechanism of coding for velocity storage, whereas the VPS neurons are likely to provide the path from the vestibular to the oculomotor system for the VO neurons.

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Orientation adaptation of eye movement–related vestibular neurons due to prolonged head tilt

Cited by 5 publications

References 21 publications

Modeling spatial tuning of adaptation of the angular vestibulo-ocular reflex

Modeling spatial tuning of adaptation of the angular vestibulo-ocular reflex

The neural basis of motion sickness

Coding of Velocity Storage in the Vestibular Nuclei

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