Vestibuloocular reflex of rhesus monkeys after spaceflight

1992 ◽  
Vol 73 (2) ◽  
pp. S121-S131 ◽  
Author(s):  
B. Cohen ◽  
I. Kozlovskaya ◽  
T. Raphan ◽  
D. Solomon ◽  
D. Helwig ◽  
...  

The vestibuloocular reflex (VOR) of two rhesus monkeys was recorded before and after 14 days of spaceflight. The gain (eye velocity/head velocity) of the horizontal VOR, tested 15 and 18 h after landing, was approximately equal to preflight values. The dominant time constant of the animal tested 15 h after landing was equivalent to that before flight. During nystagmus induced by off-vertical axis rotation (OVAR), the latency, rising time constant, steady-state eye velocity, and phase of modulation in eye velocity and eye position with respect to head position were similar in both monkeys before and after flight. There were changes in the amplitude of modulation of horizontal eye velocity during steady-state OVAR and in the ability to discharge stored activity rapidly by tilting during postrotatory nystagmus (tilt dumping) after flight: OVAR modulations were larger, and tilt dumping was lost in the one animal tested on the day of landing and for several days thereafter. If the gain and time constant of the horizontal VOR change in microgravity, they must revert to normal soon after landing. The changes that were observed suggest that adaptation to microgravity had caused alterations in way that the central nervous system processes otolith input.

2003 ◽  
Vol 13 (4-6) ◽  
pp. 377-393
Author(s):  
Steven T. Moore ◽  
Gilles Clément ◽  
Mingjai Dai ◽  
Theodore Raphan ◽  
David Solomon ◽  
...  

In this paper we review space flight experiments performed by our laboratory. Rhesus monkeys were tested before and after 12 days in orbit on COSMOS flights 2044 (1989) and 2229 (1992–1993). There was a long-lasting decrease in post-flight ocular counter-rolling (70%) and vergence (50%) during off-vertical axis rotation. In one animal, the orientation of optokinetic after-nystagmus shifted by 28° from the spatial vertical towards the body vertical early post-flight. Otolith-ocular and perceptual responses were also studied in four astronauts on the 17-day Neurolab shuttle mission (STS-90) in 1998. Ocular counter-rolling was unchanged in response to 1-g and 0.5-g Gy centrifugation during and after flight and to post-flight static roll tilts relative to pre-flight values. Orientation of the optokinetic nystagmus eye velocity axis to gravito-inertial acceleration (GIA) during centrifugation was also unaltered by exposure to microgravity. Perceptual orientation to the GIA was maintained in-flight, and subjects did not report sensation of translation during constant velocity centrifugation. These studies suggest that percepts and ocular responses to tilt are determined by sensing the body vertical relative to the GIA. The findings also raise the possibility that 'artificial gravity' during the Neurolab flight counteracted adaptation of these otolith-ocular responses.


1997 ◽  
Vol 78 (2) ◽  
pp. 1193-1197 ◽  
Author(s):  
Susan Wearne ◽  
Theodore Raphan ◽  
Bernard Cohen

Wearne, Susan, Theodore Raphan, and Bernard Cohen. Contribution of vestibular commissural pathways to spatial orientation of the angular vestibuloocular reflex. J. Neurophysiol. 78: 1193–1197, 1997. During nystagmus induced by the angular vestibuloocular reflex (aVOR), the axis of eye velocity tends to align with the direction of gravitoinertial acceleration (GIA), a process we term “spatial orientation of the aVOR.” We studied spatial orientation of the aVOR in rhesus and cynomolgus monkeys before and after midline section of the rostral medulla abolished all oculomotor functions related to velocity storage, leaving the direct optokinetic and vestibular pathways intact. Optokinetic afternystagmus and the bias component of off-vertical-axis rotation were lost, and the aVOR time constant was reduced to a value commensurate with the time constants of primary semicircular canal afferents. Spatial orientation of the aVOR, induced either during optokinetic or vestibular stimulation, was also lost. Vertical and roll aVOR time constants could no longer be lengthened in side-down or supine/prone positions, and static and dynamic tilts of the GIA no longer produced cross-coupling from the yaw to pitch and yaw to roll axes. Consequently, the induced nystagmus remained entirely in head coordinates after the lesion, regardless of the direction of the resultant GIA vector. Gains of the aVOR and of optokinetic nystagmus to steps of velocity were unaffected or slightly increased. These results are consistent with a model in which the direct aVOR pathways are organized in semicircular canal coordinates and spatial orientation is restricted to the indirect (velocity storage) pathways.


2002 ◽  
Vol 88 (5) ◽  
pp. 2445-2462 ◽  
Author(s):  
Keisuke Kushiro ◽  
Mingjia Dai ◽  
Mikhail Kunin ◽  
Sergei B. Yakushin ◽  
Bernard Cohen ◽  
...  

Nystagmus induced by off-vertical axis rotation (OVAR) about a head yaw axis is composed of a yaw bias velocity and modulations in eye position and velocity as the head changes orientation relative to gravity. The bias velocity is dependent on the tilt of the rotational axis relative to gravity and angular head velocity. For axis tilts <15°, bias velocities increased monotonically with increases in the magnitude of the projected gravity vector onto the horizontal plane of the head. For tilts of 15–90°, bias velocity was independent of tilt angle, increasing linearly as a function of head velocity with gains of 0.7–0.8, up to the saturation level of velocity storage. Asymmetries in OVAR bias velocity and asymmetries in the dominant time constant of the angular vestibuloocular reflex (aVOR) covaried and both were reduced by administration of baclofen, a GABAB agonist. Modulations in pitch and roll eye positions were in phase with nose-down and side-down head positions, respectively. Changes in roll eye position were produced mainly by slow movements, whereas vertical eye position changes were characterized by slow eye movements and saccades. Oscillations in vertical and roll eye velocities led their respective position changes by ≈90°, close to an ideal differentiation, suggesting that these modulations were due to activation of the orienting component of the linear vestibuloocular reflex (lVOR). The beating field of the horizontal nystagmus shifted the eyes 6.3°/ g toward gravity in side down position, similar to the deviations observed during static roll tilt (7.0°/ g). This demonstrates that the eyes also orient to gravity in yaw. Phases of horizontal eye velocity clustered ∼180° relative to the modulation in beating field and were not simply differentiations of changes in eye position. Contributions of orientating and compensatory components of the lVOR to the modulation of eye position and velocity were modeled using three components: a novel direct otolith-oculomotor orientation, orientation-based velocity modulation, and changes in velocity storage time constants with head position re gravity. Time constants were obtained from optokinetic after-nystagmus, a direct representation of velocity storage. When the orienting lVOR was combined with models of the compensatory lVOR and velocity estimator from sequential otolith activation to generate the bias component, the model accurately predicted eye position and velocity in three dimensions. These data support the postulates that OVAR generates compensatory eye velocity through activation of velocity storage and that oscillatory components arise predominantly through lVOR orientation mechanisms.


1995 ◽  
Vol 73 (4) ◽  
pp. 1716-1720 ◽  
Author(s):  
D. E. Angelaki ◽  
B. J. Hess

1. During rotations that dynamically activate utricular and saccular primary afferents, the otolith system centrally detects the velocity and direction of rotation of the head in space. This property is experimentally manifested as a steady-state compensatory nystagmus during constant velocity off-vertical axis rotations. The computational, physiological, and anatomic details of this response remain presently unknown. Here we report that surgical inactivation of the cerebellar nodulus and ventral uvula abolished the ability of the otolith system to generate steady-state nystagmus during constant velocity rotation and to improve the dynamics of the vestibuloocular reflex (VOR) during low-frequency sinusoidal oscillations about off-vertical axes in rhesus monkeys. These results suggest that the cerebellar nodulus and/or ventral uvula comprise part of the neural substrate that is involved in these computations.


1994 ◽  
Vol 77 (4) ◽  
pp. 1644-1652 ◽  
Author(s):  
M. Bonora ◽  
M. Boule

The influence of steady-state changes in chemical stimuli on ventilation and electromyographic activity of the diaphragm during both inspiration (total DI) and expiration (total DE) was studied in unanesthetized intact adult cats before and after carotid denervation. In intact animals, during hypercapnia (2 4, and 6% CO2), tidal volume (VT) and total DI increase, whereas total DE did not consistently change. During ambient hypocapnic hypoxia (14, 12, and 10% O2), VT increased only at 10% O2, whereas total DI increased at all levels studied. Total DE increased substantially at 14% O2, persisting up to the end of expiration with 12 and 10% O2. This effect was markedly attenuated during normocapnic hypoxia. During CO hypoxemia (1,700 ppm in air), VT as well as total DI and total DE decreased because of a large reduction in inspiratory and expiratory time elicited by tachypneic breathing. The effects of hypercapnia and hypoxia persisted after carotid denervation. Therefore, 1) in contrast to hypercapnia, hypoxia markedly enhances the expiratory diaphragmatic activity, 1) this expiratory braking mechanism depends on the severity of hypoxia and is partly due to hypocapnia secondary to hypoxia; and 3) because this effect was observed after carotid denervation and during CO hypoxemia, it may arise in the central nervous system, possibly in bulbopontine structures.


2006 ◽  
Vol 95 (3) ◽  
pp. 1571-1587 ◽  
Author(s):  
R.A.A. Vingerhoets ◽  
W. P. Medendorp ◽  
J.A.M. Van Gisbergen

Human spatial orientation relies on vision, somatosensory cues, and signals from the semicircular canals and the otoliths. The canals measure rotation, whereas the otoliths are linear accelerometers, sensitive to tilt and translation. To disambiguate the otolith signal, two main hypotheses have been proposed: frequency segregation and canal–otolith interaction. So far these models were based mainly on oculomotor behavior. In this study we investigated their applicability to human self-motion perception. Six subjects were rotated in yaw about an off-vertical axis (OVAR) at various speeds and tilt angles, in darkness. During the rotation, subjects indicated at regular intervals whether a briefly presented dot moved faster or slower than their perceived self-motion. Based on such responses, we determined the time course of the self-motion percept and characterized its steady state by a psychometric function. The psychophysical results were consistent with anecdotal reports. All subjects initially sensed rotation, but then gradually developed a percept of being translated along a cone. The rotation percept could be described by a decaying exponential with a time constant of about 20 s. Translation percept magnitude typically followed a delayed increasing exponential with delays up to 50 s and a time constant of about 15 s. The asymptotic magnitude of perceived translation increased with rotation speed and tilt angle, but never exceeded 14 cm/s. These results were most consistent with predictions of the canal–otolith-interaction model, but required parameter values that differed from the original proposal. We conclude that canal–otolith interaction is an important governing principle for self-motion perception that can be deployed flexibly, dependent on stimulus conditions.


1986 ◽  
Vol 56 (6) ◽  
pp. 1558-1570 ◽  
Author(s):  
R. D. Tomlinson ◽  
P. S. Bahra

The mechanisms of eye-head coordination were studied in two alert juvenile rhesus monkeys. Animals were trained to follow a target light to obtain a water reward and the combined eye-head gaze shifts in response to target steps with a variably sized horizontal components were studied. During a certain random portion of the gaze shifts, a torque motor was used to perturb the head to investigate the operational state of the vestibuloocular reflex (VOR) during the saccadic gaze shift. The effects of perturbing the head were assessed during five different conditions: horizontal target steps ranging from 10 to 80 degrees in amplitude; oblique target steps where the vertical component was larger than the horizontal component; purely vertical target steps 10-40 degrees in amplitude; both horizontal and oblique target steps delivered while the animals' saccades had been slowed by the use of diazepam; and large spontaneous gaze shifts in response to both sounds and visual stimuli. Comparison of perturbed and unperturbed large-amplitude (greater than 40 degrees) gaze shifts indicate that the VOR is turned off for most of the duration of the movement. Nonetheless, there is an apparent interaction between the saccadic eye movement and the head movement, thus, as the head velocity increases, the eye velocity decreases so that gaze velocity remains nearly constant throughout the gaze shift. Since the VOR is turned off when this interaction occurs, it must represent an interaction between the actual eye and head movement motor programs themselves. Although the results were not quite as clear for small saccades (less than 20 degrees), experiments on animals whose saccades had been slowed either by the use of diazepam or by combining a small horizontal component with a large vertical component indicate that the VOR is left on during these smaller gaze shifts. During quite small gaze shifts (less than 10 degrees), the VOR is clearly functioning; however, as the size of the gaze shift is increased, this becomes less clear, and there appears to be a region where the VOR operates with a gain substantially less than normal before it enters the large gaze shift region where the VOR is turned off entirely.(ABSTRACT TRUNCATED AT 400 WORDS)


1975 ◽  
Vol 43 (6) ◽  
pp. 717-720 ◽  
Author(s):  
James L. Picardi ◽  
H. Paul Lewis ◽  
James S. Tan ◽  
John P. Phair

✓ The authors measured levels of clindamycin, a drug well established as useful in the treatment of various soft-tissue and parenchymal bacterial infections, in serum, cerebrospinal fluid, and brain tissue of 14 rhesus monkeys. Penetration into brain tissue was erratic and concentrations detected were not significant. Cerebrospinal fluid levels, however, averaged 20.5% of paired serum concentrations and were higher than concentrations needed to inhibit most Gram-positive bacteria. Further studies in humans are indicated before this antibiotic may be used routinely.


1994 ◽  
Vol 72 (3) ◽  
pp. 1383-1394 ◽  
Author(s):  
A. M. Pastor ◽  
R. R. de la Cruz ◽  
R. Baker

1. The time course of eye velocity responses elicited by head velocity steps was compared in normal, adapted, and cerebellectomized goldfish. Vestibuloocular reflex (VOR) adaptation was induced by combined visual and vestibular stimulation that altered the ratio of eye to head velocity (VOR gain) toward values either higher or lower than the control amplitude. The velocity step consisted of alternating periods of head rotation at a constant velocity of 16 degrees/s zero-to-peak around the vertical axis. 2. The VOR produced by head velocity steps consisted of an early acceleration-related component, the dynamic response, separated from a sustained period of constant velocity, the plateau, by a sag that occurred around 125-150 ms. Latency of the VOR averaged 18 ms for the adducting eye and 20 ms for abducting eye independent of the initial VOR gain. Adapted dynamic VOR responses diverged from the control records at the earliest detectable latency after both high and low VOR gain training. This result demonstrates modification in the shortest latency brain stem VOR pathway, presumably, the three-neuron reflex arc. 3. After acute cerebellectomy the adapted dynamic response was unaltered for approximately 50 ms in the low-gain and 70 ms in the high-gain VOR states. Not less than 30% of the altered velocity was retained throughout the remaining dynamic and sustained component. These results demonstrate that the vestibulocerebellum is not necessary for the maintenance of the earliest adapted eye velocity. Hence brain stem pathways are sufficient for the expression of the modified VOR. 4. Purkinje cells identified by simple and complex spikes were recorded extracellularly in the area of the vestibulocerebellum, where electrical stimulation produced conjugate ipsiversive horizontal eye movements. Independent eye and head velocity sensitivities were determined in response to visual world motion and VOR suppression, respectively. The two signals either added, canceled, or were both present in Purkinje cells throughout the range of eye velocity induced by vertical axis visual-vestibular stimulation. 5. Latency of Purkinje cell discharge to either a vestibular or visual velocity step exhibited means of 43 and 70 ms, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)


2002 ◽  
Vol 87 (2) ◽  
pp. 1159-1164 ◽  
Author(s):  
J. Eric Killian ◽  
James F. Baker

The horizontal vestibuloocular reflex (VOR) of Purkinje cell degeneration ( pcd/pcd) mutant mice, which lack a functional cerebellar cortex, was compared in darkness to that of wild-type animals during constant velocity yaw rotations about an earth-horizontal axis and during sinusoidal yaw rotations about an earth-vertical axis. Both wild-type and pcd/pcd mice showed a compensatory average VOR eye velocity, or bias, during constant velocity horizontal axis rotations, evidence of central neural processing of otolith afferent signals to create a signal proportional to head angular velocity. Eye velocity bias was greater in pcd/pcd mice than in wild-type mice at a low rotational velocity (32°/s), but less at higher velocities (128 and 200°/s). Lesion of the medial nodulus severely attenuated eye velocity bias in two wild-type mice, without attenuating VOR during sinusoidal vertical axis yaw rotations at 0.2 Hz. These results show that while head velocity estimation in mice, as in primates, depends on the cerebellum, pcd/pcd mutant mice develop velocity estimation without a functional cerebellar cortex. We conclude that neural circuits that exclude cerebellar cortex are capable of the signal processing necessary for head angular velocity estimation, but that these circuits are insufficient for normal estimation at high velocities.


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