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S B Yakushin

Publications and source records attributed to S B Yakushin.

10 recordsLinked to original sources
PubMed2001

Changes in the vestibulo-ocular reflex after plugging of the semicircular canals.

The gain of the angular vestibulo-ocular reflex (aVOR) was determined in monkeys by rotation about a spatial vertical axis while upright or statically tilted forward and backward. Horizontal, vertical, and roll gains were determined at each head orientation and plotted as a function of head tilt. Before canal plugging, animals had maximal (spatial) horizontal gains when upright (spatial phase 0 degrees) and maximal roll gains when tilted forward or backward 90 degrees. Plugging caused striking changes in the characteristics of the aVOR gains at low frequencies. After plugging of the vertical canals, maximal horizontal and roll gains both occurred at head tilts of approximately 30 degrees forward. When the lateral canals were plugged, maximal horizontal and roll responses occurred when the head was tilted back approximately 50 degrees. The aVOR gains of the canal-plugged animals were also affected by stimulus frequency. In every instance, as stimulus frequency increased, the spatial phases shifted toward the normal response, that is, the response before plugging. This normalization effect was observed even in the animals with all six semicircular canals plugged, indicating that normalization was not due to spatial adaptation. A three-dimensional dynamic and kinematic model of the aVOR was able to account for all types of canal plugging by a simple change in the dominant time constant of the plugged canals from 3 s to 5 s to approximately 0.07 s. The model accurately predicted responses of the normal and canal-plugged animals at all frequencies. These data show that the central vestibular system does not spatially adapt to losses resulting from canal plugging.

Animals↗
PubMed2000

Functions of the nucleus of the optic tract (NOT). II. Control of ocular pursuit.

Ocular pursuit in monkeys, elicited by sinusoidal and triangular (constant velocity) stimuli, was studied before and after lesions of the nucleus of the optic tract (NOT). Before NOT lesions, pursuit gains (eye velocity/target velocity) were close to unity for sinusoidal and constant-velocity stimuli at frequencies up to 1 Hz. In this range, retinal slip was less than 2 degrees. Electrode tracks made to identify the location of NOT caused deficits in ipsilateral pursuit, which later recovered. Small electrolytic lesions of NOT reduced ipsilateral pursuit gains to below 0.5 in all tested conditions. Pursuit was better, however, when the eyes moved from the contralateral side toward the center (centripetal pursuit) than from the center ipsilaterally (centrifugal pursuit), although the eyes remained in close proximity to the target with saccadic tracking. Effects of lesions on ipsilateral pursuit were not permanent, and pursuit gains had generally recovered to 60-80% of baseline after about 2 weeks. One animal had bilateral NOT lesions and lost pursuit for 4 days. Thereafter, it had a centrifugal pursuit deficit that lasted for more than 2 months. Vertical pursuit and visually guided saccades were not affected by the bilateral NOT lesions in this animal. We also compared effects of these and similar NOT lesions on optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN). Correlation of functional deficits with NOT lesions from this and previous studies showed that rostral lesions of NOT in and around the pretectal olivary nucleus, which interrupted cortical input through the brachium of the superior colliculus (BSC), affected both smooth pursuit and OKN. In two animals in which it was tested, NOT lesions that caused a deficit in pursuit also decreased the rapid and slow components of OKN slow-phase velocity and affected OKAN. It was previously shown that slightly more caudal NOT lesions were more effective in altering gain adaptation of the angular vestibulo-ocular reflex (aVOR). The present findings suggest that cortical pathways through rostral NOT play an important role in maintenance of ipsilateral ocular pursuit. Since lesions that affected ocular pursuit had similar effects on ipsilateral OKN, processing for these two functions is probably closely linked in NOT, as it is elsewhere.

Animals↗
PubMed2000

Functions of the nucleus of the optic tract (NOT). I. Adaptation of the gain of the horizontal vestibulo-ocular reflex.

We studied the role of the nucleus of the optic tract (NOT) in adapting the gain of the angular vestibulo-ocular reflex (aVOR) in rhesus and cynomolgus monkeys using lesions and temporary inactivation with muscimol. The aVOR gain was adaptively reduced by forced sinusoidal rotation (0.25 Hz, 60 degrees/s) in a self-stationary visual surround, i.e., a visual surround that moved with the subject, or by wearing x0.5 reducing lenses during natural head movements. The aVOR gains dropped by 20-30% after 2 h and by about 30% after 4 h. Muscimol injections caused a loss of adaptation of contraversive-eye velocities induced by the aVOR, and their gains promptly returned to or above preadapted levels. The gains of the adapted ipsiversive and vertical eye velocities produced by the aVOR were unaffected by muscimol injections. Lesions of NOT significantly reduced or abolished the animals' ability to adapt the gain of contraversive aVOR-induced eye velocities, and the monkeys were unable to suppress these contraversive-eye velocities in a self-stationary surround. The lesions did not affect ipsiversive aVOR-induced eye velocities, and the animals were still able to suppress them. Lesions of NOT also affected the unadapted or "default" aVOR gains. After unilateral NOT lesions, gains of ipsiversive aVOR-induced eye velocity were reduced, while gains of contraversive aVOR-induced eye velocity were either unaffected or slightly increased. Consistent with this, muscimol injections into the NOT of unadapted monkeys slightly reduced the gains of ipsiversive and increased the gains of contraversive-eye velocities by about 8-10%. We conclude that each NOT processes ipsiversive retinal-slip information about visual surround movement relative to the head induced by the aVOR. In the presence of visual surround movement, the retinal-slip signal is suppressed, leading to adaptive changes in the gain of aVOR-induced contraversive horizontal eye velocities. NOT also has a role in controlling and maintaining the current state of the aVOR gains. Thus, it plays a unique role in producing and supporting adaptation of the gain of the horizontal aVOR that is likely to be important for stabilizing gaze during head movement. Pathways through the inferior olive are presumably important for this adaptation.

Adaptation, Physiological↗
PubMed2000

Context-specific adaptation of the vertical vestibuloocular reflex with regard to gravity.

We determined whether head position with regard to gravity is an important context for angular vestibuloocular reflex (aVOR) gain adaptation. Vertical aVOR gains were adapted with monkeys upright or on side by rotating the animals about an interaural axis in phase or out of phase with the visual surround for 4 h. When aVOR gains were adapted with monkeys upright, gain changes were symmetrical when tested in either on-side position (23 +/- 7%; mean +/- SD). After on-side adaptation, however, gain changes were always larger when animals were tested in the same on-side position in which they were adapted. Gain changes were 43 +/- 16% with ipsilateral side down and 9 +/- 8% with contralateral side down. The context-specific effects of head position on vertical aVOR gain were the same whether the gain was increased or decreased. The data indicate that vertical aVOR gain changes are stored in the context of the head orientation in which changes were induced. This association could be an important context for expressing the adapted state of the aVOR gain during vertical head movement.

Adaptation, Physiological↗
PubMed1999

Control of spatial orientation of the angular vestibulo-ocular reflex by the nodulus and uvula of the vestibulocerebellum.

Eye velocity produced by the angular vestibulo-ocular reflex (aVOR) tends to align with the summed vector of gravity and other linear accelerations [gravito-inertial acceleration (GIA)]. Defined as "spatial orientation of the aVOR," we propose that it is controlled by the nodulus and uvula of the vestibulocerebellum. Here, electrical stimulation, injections of the GABAA agonist, muscimol, and single-cell recordings were utilized to investigate this spatial orientation. Stimulation, injection, and recording sites in the nodulus were determined in vivo by MRI and verified in histological sections. MRI proved to be a sensitive, reliable way to localize electrode placements. Electrical stimulation at sites in the nodulus and sublobule d of the uvula produced nystagmus whose slow-phase eye-velocity vectors were either head centric or spatially invariant. When head centric, the eye velocity vector remained within +/- 45 degrees of the vector obtained with the animal upright, regardless of head position with respect to gravity. When spatially oriented, the vector remained relatively constant in space in one on-side position, with respect to the vector determined with the animal upright. A majority of induced movements from the nodulus were spatially oriented. Spatially oriented movements were generally followed by after-nystagmus, which had the characteristics of optokinetic after-nystagmus (OKAN), including orientation to the GIA. After muscimol injections, horizontal-to-vertical cross-coupling was lost or reduced during OKAN in tilted positions. This supports the hypothesis that the nodulus mediates yaw-to-vertical or roll cross-coupling. The injections also shortened the yaw-axis time constant and produced contralateral horizontal spontaneous nystagmus, whose velocity varied as a function of head position with regard to gravity. Nodulus units were tested with static head tilt, sinusoidal oscillation around a spatial horizontal axis with the head in different orientations relative to the pitching plane, and off-vertical axis rotation (OVAR). The direction of the response vectors of the otolith-recipient units in the nodulus, determined from static and/or dynamic head tilts, were confirmed by OVAR. These vector directions lay close to the planes of the vertical canals in 7/10 units; many units also had convergent input from the vertical canals. It is postulated that the orientation properties of the aVOR result from a transfer of otolith input regarding head tilt along canal planes to canal-related zones of the nodulus. In turn, Purkinje cells in these zones project to vestibular nuclei neurons to control eye velocity around axes normal to these same canal planes.

Animals↗
PubMed1998

Dynamics and kinematics of the angular vestibulo-ocular reflex in monkey: effects of canal plugging.

Dynamics and kinematics of the angular vestibulo-ocular reflex in monkey: effects of canal plugging. J. Neurophysiol. 80: 3077-3099, 1998. Horizontal and roll components of the angular vestibulo-ocular reflex (aVOR) were elicited by sinusoidal rotation at frequencies from 0.2 Hz (60 degrees/s) to 4.0 Hz ( approximately 6 degrees/s) in cynomolgus monkeys. Animals had both lateral canals plugged (VC, vertical canals intact), both lateral canals and one pair of the vertical canals plugged (RALP, right anterior and left posterior canals intact; LARP, left anterior and right posterior canal intact), or all six semicircular canal plugged (NC, no canals). In normal animals, horizontal and roll eye velocity was in phase with head velocity and peak horizontal and roll gains were approximately 0.8 and 0.6 in upright and 90 degrees pitch, respectively. NC animals had small aVOR gains at 0.2 Hz, and the temporal phases were shifted approximately 90 degrees toward acceleration. As the frequency increased to 4 Hz, aVOR temporal gains and phases tended to normalize. Findings were similar for the LARP, RALP, and VC animals when they were rotated in the planes of the plugged canals. That is, they tended to normalize at higher frequencies. A model was developed incorporating the geometric organization of the canals and first order canal-endolymph dynamics. Canal plugging was modeled as an alteration in the low frequency 3-db roll-off and corresponding dominant time constant. The shift in the low-frequency 3-dB roll-off was seen in the temporal responses as a phase lead of the aVOR toward acceleration at higher frequencies. The phase shifted toward stimulus velocity as the frequency increased toward 4.0 Hz. By incorporating a dynamic model of the canals into the three-dimensional canal system, the spatial responses were predicted at all frequencies. Animals were also stimulated with steps of velocity in planes parallel to the plugged lateral canals. This induced a response with a short time constant and low peak velocity in each monkey. Gains were normalized for step rotation with respect to time constant as (steady state eye velocity)/(stimulus acceleration x time constant). Using this procedure, the gains were the same in canal plugged as in normal animals and corresponded to gains obtained in the frequency analysis. The study suggests that canal plugging does not block the afferent response to rotation, it merely shifts the dynamic response to higher frequencies.

Algorithms↗
PubMed1992

Changes in monkey horizontal semicircular canal afferent responses after spaceflight.

Extracellular responses from single horizontal semicircular canal afferents in two rhesus monkeys were studied after recovery from a 14-day biosatellite (COSMOS 2044) orbital spaceflight. On the 1st postflight day, the mean gain for 9 different horizontal canal afferents, tested using one or several different passive yaw rotation waveforms, was nearly twice that for 20 horizontal canal afferents similarly tested during preflight and postflight control studies. Adaptation of the afferent response to passive yaw rotation on the 1st postflight day was also greater. These results suggest that at least one component of the vestibular end organ (the semicircular canals) is transiently modified after exposure to 14 days of microgravity. It is unclear whether the changes are secondary to other effects of microgravity, such as calcium loss, or an adaptive response. If the response is adaptive, then this report is the first evidence that the response of the vestibular end organ may be modified (presumably by the central nervous system via efferent connections) after prolonged unusual vestibular stimulation. If this is the case, the sites of plasticity of vestibular responses may not be exclusively within central nervous system vestibular structures, as previously believed.

Adaptation, Physiological↗