Role of the Y Group of the Vestibular Nuclei in Motor Learning or Plasticity of the Vestibulo-Ocular Reflex in the Squirrel Monkey

1996 ◽  
Vol 781 (1 Lipids and Sy) ◽  
pp. 513-524 ◽  
Author(s):  
A. M. PARTSALIS ◽  
STEPHEN M. HIGHSTEIN
eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Rhea R Kimpo ◽  
Jacob M Rinaldi ◽  
Christina K Kim ◽  
Hannah L Payne ◽  
Jennifer L Raymond

Cerebellar climbing fiber activity encodes performance errors during many motor learning tasks, but the role of these error signals in learning has been controversial. We compared two motor learning paradigms that elicited equally robust putative error signals in the same climbing fibers: learned increases and decreases in the gain of the vestibulo-ocular reflex (VOR). During VOR-increase training, climbing fiber activity on one trial predicted changes in cerebellar output on the next trial, and optogenetic activation of climbing fibers to mimic their encoding of performance errors was sufficient to implant a motor memory. In contrast, during VOR-decrease training, there was no trial-by-trial correlation between climbing fiber activity and changes in cerebellar output, and climbing fiber activation did not induce VOR-decrease learning. Our data suggest that the ability of climbing fibers to induce plasticity can be dynamically gated in vivo, even under conditions where climbing fibers are robustly activated by performance errors.


2004 ◽  
Vol 3 (3) ◽  
pp. 188-192 ◽  
Author(s):  
Pablo Blazquez ◽  
Yutaka Hirata ◽  
Stephen Highstein

1999 ◽  
Vol 9 (3) ◽  
pp. 163-172
Author(s):  
Bernard Cohen ◽  
Susan Wearne ◽  
Mingjia Dai ◽  
Theodore Raphan

During vestibular nystagmus, optokinetic nystagmus (OKN), and optokinetic afternystagmus (OKAN), the axis of eye rotation tends to align with the vector sum of linear accelerations acting on the head. This includes gravitational acceleration and the linear accelerations generated by translation and centrifugation. We define the summed vector of gravitational and linear accelerations as gravito-inertial acceleration (GIA) and designate the phenomenon of alignment as spatial orientation of the angular vestibuloocular reflex (aVOR). On the basis of studies in the monkey, we postulated that the spatial orientation of the aVOR is dependent on the slow (velocity storage) component of the aVOR, not on the short latency, compensatory aVOR component, which is in head-fixed coordinates. Experiments in which velocity storage was abolished by midline medullary section support this postulate. The velocity storage component of the aVOR is likely to be generated in the vestibular nuclei, and its spatial orientation was shown to be controlled through the nodulus and uvula of the vestibulo-cerebellum. Separate regions of the nodulus/uvula appear to affect the horizontal and vertical/torsional components of the response differently. Velocity storage is weaker in humans than in monkeys, but responds in a similar fashion in both species. We postulate that spatial orientation of the aVOR plays an important role in aligning gaze with the GIA and in maintaining balance during angular locomotion.


2019 ◽  
Vol 30 (09) ◽  
pp. 792-801 ◽  
Author(s):  
Mary Easterday ◽  
Patrick N. Plyler ◽  
James D. Lewis ◽  
Steven M. Doettl

AbstractAccurate vestibulo-ocular reflex (VOR) measurement requires control of extravestibular suppressive factors such as visual fixation. Although visual fixation is the dominant suppressor and has been extensively studied, the mechanisms underlying suppression from nonvisual factors of attention and auditory stimulation are less clear. It has been postulated that the nonvisual suppression of the VOR is the result of one of two mechanisms: (1) activation of auditory reception areas excites efferent pathways to the vestibular nuclei, thus inhibiting the VOR or (2) cortical modulation of the VOR results from directed attention, which implies a nonmodality-specific process.The purpose of this research was to determine if the VOR is affected by the intensity level and/or type of speech stimulus.A repeated measures design was used. The experiment was single-blinded.Participants included 17 adults (14 females, three males) between the ages of 18–34 years who reported normal oculomotor, vestibular, neurological, and musculoskeletal function.Each participant underwent slow harmonic acceleration testing in a rotational chair. VOR gain was assessed at 0.02, 0.08, and 0.32 Hz in quiet (baseline). VOR gain was also assessed at each frequency while a forward running speech stimulus (attentional) or a backward running speech stimulus (nonattentional) was presented binaurally via insert earphones at 42, 62, and 82 dBA. The order of the conditions was randomized across participants. VOR difference gain was calculated as VOR gain in the auditory condition minus baseline VOR gain. To evaluate auditory efferent function, the medial olivocochlear reflex (MOCR) was assayed using transient-evoked otoacoustic emissions (right ear) measured in the presence and absence of broadband noise (left ear). Contralateral acoustic reflex thresholds were also assessed using a broadband noise elicitor. A three-way repeated measures analysis of variance was conducted to evaluate the effect of frequency, intensity level, and speech type on VOR difference gain. Correlations were conducted to determine if difference gain was related to the strength of the MOCR and/or to the acoustic reflex threshold.The analysis of variance indicated that VOR difference gain was not significantly affected by the intensity level or the type of speech stimulus. Correlations indicated VOR difference gain was not significantly related to the strength of the MOCR or the acoustic reflex threshold.The results were in contrast to previous research examining the effect of auditory stimulation on VOR gain as auditory stimulation did not produce VOR suppression or enhancement for most of the participants. Methodological differences between the studies may explain the discrepant results. The removal of an acoustic target from space to attend to may have prevented suppression or enhancement of the VOR. Findings support the hypothesis that VOR gain may be affected by cortical modulation through directed attention rather than due to activation of efferent pathways to the vestibular nuclei.


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