Physiologic basis for motor learning in the vestibulo-ocular reflex

1998 ◽  
Vol 119 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Stephen G. Lisberger
Keyword(s):  
Purkinje Cells ◽  
Cerebellar Cortex ◽  
Neural Circuits ◽  
Vestibular Nuclei ◽  
Neural Mechanisms ◽  
Cellular Mechanisms ◽  
Ocular Reflex ◽  
Monosynaptic Inhibition ◽  
Vestibulo Ocular Reflex ◽  
Head Neck

The vestibulo-ocular reflex has been used extensively for study of the neural mechanisms of learning that is dependent on an intact cerebellum. Anatomic, physiologic, behavioral, and computational approaches have revealed the neural circuits that are used to generate the vestibulo-ocular reflex and have identified two likely sites of plasticity within those circuits. One site of plasticity is in the vestibular inputs to floccular target neurons, which are located in the vestibular nuclei and receive monosynaptic inhibition from Purkinje cells in the floccular complex of the cerebellar cortex. The other site of plasticity is in the vestibular inputs to Purkinje cells in the floccular complex, possibly in the cerebellar cortex. After reviewing the evidence that supports these conclusions, I consider a number of observations showing that the dynamics of neural circuits or cellular mechanisms play important roles in learning in the vestibulo-ocular reflex. (Otolaryngol Head Neck Surg 1998;119:43–8.)

Spatial orientation of the angular vestibulo-ocular reflex

1999 ◽  
Vol 9 (3) ◽  
pp. 163-172
Author(s):  
Bernard Cohen ◽  
Susan Wearne ◽  
Mingjia Dai ◽  
Theodore Raphan
Keyword(s):  
Spatial Orientation ◽  
Optokinetic Nystagmus ◽  
Vestibular Nuclei ◽  
Velocity Storage ◽  
Gravitational Acceleration ◽  
Ocular Reflex ◽  
Eye Rotation ◽  
Slow Velocity ◽  
Vestibulo Ocular Reflex ◽  
Vector Sum

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.

scholarly journals Effect of Intensity Level and Speech Stimulus Type on the Vestibulo-Ocular Reflex

2019 ◽  
Vol 30 (09) ◽  
pp. 792-801 ◽  
Author(s):  
Mary Easterday ◽  
Patrick N. Plyler ◽  
James D. Lewis ◽  
Steven M. Doettl
Keyword(s):  
Repeated Measures ◽  
Vestibular Nuclei ◽  
Auditory Stimulation ◽  
Broadband Noise ◽  
Speech Stimulus ◽  
Intensity Level ◽  
Acoustic Reflex ◽  
Ocular Reflex ◽  
Vestibulo Ocular Reflex ◽  
Acoustic Reflex Threshold

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.

Anterior canal neurons in cat vestibular nuclei have large phase leads during low frequency vertical axis pitch

2007 ◽  
Vol 16 (6) ◽  
pp. 245-256
Author(s):  
Sandra C. Brettler ◽  
James F. Baker
Keyword(s):  
Low Frequency ◽  
Vertical Axis ◽  
Vestibular Nuclei ◽  
Whole Body ◽  
Posterior Canal ◽  
Spatial Sensitivity ◽  
Ocular Reflex ◽  
Vestibular Afferents ◽  
Vestibulo Ocular Reflex ◽  
Anterior Canal

Vestibulo-ocular and second-order neurons in medial and superior vestibular nuclei of alert cats were identified by antidromic and orthodromic electrical stimulation, and their responses to whole body rotations were recorded in the dark. Neurons that had spatial sensitivity most closely aligned with the anterior canal (anterior canal neurons) were compared with neurons that had spatial sensitivity most closely aligned with the posterior canal (posterior canal neurons). Responses were recorded during low frequency earth-horizontal axis pitch rotations in the normal upright posture, and during earth-vertical axis pitch with the head and body lying on the left side. During upright pitch, response phases of anterior canal neurons slightly lagged those of posterior canal neurons or primary vestibular afferents, as previously reported. During on-side pitch, anterior canal neurons showed far greater phase leads with respect to head velocity than posterior canal neurons, primary vestibular afferents, or previously reported vestibulo-ocular reflex eye movements. These results provide challenges for vestibulo-ocular reflex models to incorporate central mechanisms for phase leads among the inputs to anterior canal neurons and to explain how the anterior canal neuron signals reported here combine with other signals to produce observed vestibulo-ocular reflex behavior.

scholarly journals Differential Purkinje cell simple spike activity and pausing behavior related to cerebellar modules

2015 ◽  
Vol 113 (7) ◽  
pp. 2524-2536 ◽  
Author(s):  
Haibo Zhou ◽  
Kai Voges ◽  
Zhanmin Lin ◽  
Chiheng Ju ◽  
Martijn Schonewille
Keyword(s):  
Purkinje Cell ◽  
Purkinje Cells ◽  
Cerebellar Cortex ◽  
Spike Activity ◽  
Vestibular Nuclei ◽  
Simple Spike ◽  
Transverse Zone ◽  
Cerebellar Modules ◽  
Lower Temperature ◽  
Cerebellar Purkinje Cells

The massive computational capacity of the cerebellar cortex is conveyed by Purkinje cells onto cerebellar and vestibular nuclei neurons through their GABAergic, inhibitory output. This implies that pauses in Purkinje cell simple spike activity are potentially instrumental in cerebellar information processing, but their occurrence and extent are still heavily debated. The cerebellar cortex, although often treated as such, is not homogeneous. Cerebellar modules with distinct anatomical connectivity and gene expression have been described, and Purkinje cells in these modules also differ in firing rate of simple and complex spikes. In this study we systematically correlate, in awake mice, the pausing in simple spike activity of Purkinje cells recorded throughout the entire cerebellum, with their location in terms of lobule, transverse zone, and zebrin-identified cerebellar module. A subset of Purkinje cells displayed long (>500-ms) pauses, but we found that their occurrence correlated with tissue damage and lower temperature. In contrast to long pauses, short pauses (<500 ms) and the shape of the interspike interval (ISI) distributions can differ between Purkinje cells of different lobules and cerebellar modules. In fact, the ISI distributions can differ both between and within populations of Purkinje cells with the same zebrin identity, and these differences are at least in part caused by differential synaptic inputs. Our results suggest that long pauses are rare but that there are differences related to shorter intersimple spike intervals between and within specific subsets of Purkinje cells, indicating a potential further segregation in the activity of cerebellar Purkinje cells.

Noradrenergic influences on the cerebellar cortex: Effects on vestibular reflexes under basic and adaptive conditions

1998 ◽  
Vol 119 (1) ◽  
pp. 93-105 ◽  
Author(s):  
Ottavio Pompeiano
Keyword(s):  
Purkinje Cells ◽  
Immediate Early Genes ◽  
Visual Signals ◽  
Immediate Early ◽  
Vestibular Reflexes ◽  
Opposite Result ◽  
Early Genes ◽  
Ocular Reflex ◽  
Vestibulo Ocular Reflex

Experiments performed either in decerebrate cats or in intact rabbits have shown that functional inactivation of the cerebellar anterior vermis or the flocculus decreased the basic gain of the vestibulospinal or the vestibulo-ocular reflex, respectively. These findings were attributed to the fact that a proportion of the vermal or floccular Purkinje cells, which are inhibitory in function, discharge out of phase with respect to the vestibulospinal or the vestibulo-ocular neurons during sinusoidal animal rotation, thus exerting a facilitatory influence on the gain of the vestibular reflexes. Intravermal injection of a β-noradrenergic agonist slightly increased the gain of the vestibulospinal reflex, whereas the opposite result was obtained after injection of β-antagonists. Similarly, intrafloccular injection of a β-noradrenergic agonist slightly facilitated the gain of the vestibulo-ocular reflex in darkness (but not in light), whereas a small decrease of the reflex occurred after injection of a β-antagonist. It was postulated that the noradrenergic system acts on Purkinje cells by enhancing their amplitude of modulation to a given labyrinth signal, thus increasing the basic gain of the vestibular reflexes. The Purkinje cells of the cerebellar anterior vermis and the flocculus also exert a prominent role on the adaptation of vestibulospinal and vestibulo-ocular reflexes, respectively. In particular, intravermal or intrafloccular injection of β-noradrenergic antagonists decreased or suppressed the adaptive capacity of the vestibulospinal and vestibulo-ocular reflexes that always occurred during sustained out-of-phase neck-vestibular or visual-vestibular stimulation, whereas the opposite result was obtained after local injection of a β-noradrenergic agonist. The noradrenergic innervation of the cere-bellar cortex originates from the locus coeruleus complex, whose neurons respond to vestibular, neck, and visual signals. It was postulated that this structure acts through β-adrenoceptors to increase the expression of immediate-early genes, such as c- fos and Jun-B, in the Purkinje cells during vestibular adaptation. Induction of immediate-early genes could then represent a mechanism by which impulses elicited by sustained neck-vestibular or visuovestibular stimulation are transduced into long-term biochemical changes that are required for cerebellar long-term plasticity. (Otolaryngol Head Neck Surg 1998;119:93-105.)

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