Eye movements induced by pontine stimulation: interaction with visually triggered saccades

1987 ◽  
Vol 58 (2) ◽  
pp. 300-318 ◽  
Author(s):  
D. L. Sparks ◽  
L. E. Mays ◽  
J. D. Porter
Keyword(s):  
Visual Target ◽  
Motor Command ◽  
Feedback Signal ◽  
Eye Position ◽  
Saccadic System ◽  
Position Signal ◽  
Orbital Position ◽  
A Site ◽  
Induced Changes ◽  
Pontine Stimulation

1. Rhesus monkeys were trained to look to brief visual targets presented in an otherwise darkened room. On some trials, after the visual target was extinguished but before a saccade to it could be initiated, the eyes were driven to another orbital position by microstimulation of the paramedian pontine reticular formation. If, as current models of the saccadic system suggest, a copy of the motor command is used as a feedback signal of eye position, failure to compensate for stimulation-induced movements would indicate that stimulation occurred at a site beyond the point from which the eye position signal was derived. 2. Animals compensated for perturbations of eye position induced by stimulation of most pontine sites by making saccades that directed gaze to the position of the visual target. With stimulation at other pontine sites, compensatory saccades did not occur. 3. Pontine stimulation sometimes triggered, prematurely, impending visually directed saccades. The direction and amplitude of the premature movement depended upon the location of the briefly presented visual target. The amplitude of the premature movement was also a function of the interval between the stimulation train and the impending saccade. These data suggest that input signals for the horizontal and vertical pulse/step generators develop gradually during the presaccadic interval. Saccade trigger signals need to be delayed until the formation of these signals is completed. 4. The implications of these findings for models of the saccadic system are discussed. Robinson's local feedback model of the saccadic system can explain compensation for pontine stimulation-induced changes in eye position but cannot easily account for the failure to compensate for perturbations in eye position produced by stimulation at other sites. Modified versions of Robinson's model, which assume that the input signal to the pulse/step generator is the desired displacement of the eye, can account for both compensation and the failure to compensate since two separate neural integrators are employed. However, these models ignore kinematic arguments that commands to the extraocular muscles must specify the absolute position of the eye in the orbit rather than a relative movement from a previous position.

Mislocalisation of Chromatic and Achromatic Stimuli during Saccadic Eye Movements

Perception ◽  
1996 ◽  
Vol 25 (1_suppl) ◽  
pp. 137-137
Author(s):  
M Sato ◽  
K Uchikawa
Keyword(s):  
Eye Movements ◽  
Opposite Direction ◽  
Visual Target ◽  
Saccadic Eye Movements ◽  
Eye Position ◽  
Stationary Target ◽  
Actual Position ◽  
Chromatic Stimulus ◽  
Position Signal ◽  
Retinal Information

It is well known that a brief flash of a small stationary target presented during saccades appears to be shifted from the actual position. The perceptual location of a visual target should be determined by the retinal information and the eye position signal. This mislocalisation seems to indicate that the change of the eye position signal is more sluggish than the actual eye movements. Delay of transmission of the retinal information may be a factor of mislocalisation. Here, we measured the perceptual location of chromatic stimuli which had different temporal characteristics from achromatic stimuli. The chromatic stimulus was a small red spot which replaced the green field for 10 ms. The green field subtended 5 deg × 24 deg and its luminance was 78.6 cd m−2. The luminance of the chromatic stimulus was adjusted to be the same as the green field by the minimum flicker method. The luminance of the achromatic stimulus was 234 cd m−2. Our results show that the chromatic and the achromatic stimuli presented at the beginning of saccades are mislocalised in the same direction as the saccades. We also found that the mislocalisation of the chromatic stimulus began slightly earlier than the achromatic stimulus. Also the chromatic stimulus presented during saccades was mislocalised in the opposite direction to the saccades whereas the achromatic stimulus was localised approximately at the actual position. These results suggest that the chromatic response is transmitted more slowly before saccades but faster during saccades than the achromatic response.

Human Sound-Localization Behavior Accounts for Ocular Drift

2010 ◽  
Vol 103 (4) ◽  
pp. 1927-1936 ◽  
Author(s):  
Tom J. Van Grootel ◽  
A. John Van Opstal
Keyword(s):  
Motor Command ◽  
Head Position ◽  
Eye Position ◽  
Neutral Position ◽  
Neural Integrator ◽  
Complete Darkness ◽  
Sound Location ◽  
Position Signal ◽  
Localization Errors ◽  
Localization Behavior

To generate an accurate saccade toward a sound in darkness requires a transformation of the head-centered sound location into an oculocentric motor command, which necessitates the use of an eye-in-head position signal. We tested whether this transformation uses a continuous representation of eye position by exploiting the property that the oculomotor neural integrator is leaky with a time constant of ∼20 s. Hence in complete darkness, the eyes tend to drift toward a neutral position. Alternatively, the spatial mapping stage could employ a sampled eye-position signal in which case drift will not be accounted for. Our data show that the sound location is accurately represented and that the transformation uses a dynamic eye-position signal. This signal, however, is slightly underestimated, leading to small systematic localization errors that tend to covary with the direction of eye position.

Effect of Diamagnetic A2+ Substitution on the Magnetic and Ferroelectric Properties of the Bi1−xAxFeO3 Multiferroics

2007 ◽  
Vol 1034 ◽  
Author(s):  
V. A. Khomchenko ◽  
D. A. Kiselev ◽  
J. M. Vieira ◽  
Li Jian ◽  
A. M. L. Lopes ◽  
...  
Keyword(s):  
Spin Structure ◽  
Ionic Radius ◽  
Ferroelectric Properties ◽  
Piezoresponse Force Microscopy ◽  
Weak Ferromagnetism ◽  
Force Microscopy ◽  
Microscopy Data ◽  
A Site ◽  
Induced Changes ◽  
Spiral Spin

AbstractInvestigation of crystal structure, magnetic and local ferroelectric properties of the diamagnetically-doped Bi1−xAxFeO3 (A= Ca, Sr, Pb, Ba; x= 0.2, 0.3) ceramic samples has been carried out. It has been shown that the solid solutions have a rhombohedrally distorted perovskite structure described by the space group R3c. Piezoresponse force microscopy data have revealed the existence of the spontaneous ferroelectric polarization in the samples at room temperature. Magnetization measurements have shown that the magnetic state of these compounds is determined by the ionic radius of the substituting elements. A-site substitution with the biggest ionic radius ions has been found to suppress the spiral spin structure of BiFeO3 and to result in the appearance of weak ferromagnetism. The magnetic properties have been discussed in terms of doping- induced changes in the magnetic anisotropy.

scholarly journals Comparison of Two Methods of Producing Adaptation of Saccade Size and Implications for the Site of Plasticity

1998 ◽  
Vol 79 (2) ◽  
pp. 704-715 ◽  
Author(s):  
Charles A. Scudder ◽  
Ekatherina Y. Batourina ◽  
George S. Tunder
Keyword(s):  
Relative Size ◽  
Neural Mechanisms ◽  
The Other ◽  
Rapid Adaptation ◽  
Adaptive Mechanisms ◽  
Saccade Size ◽  
Orbital Position ◽  
One Step ◽  
Induced Changes ◽  
Visual Error

Scudder, Charles A., Ekatherina Y. Batourina, and George S. Tunder. Comparison of two methods of producing adaptation of saccade size and implications for the site of plasticity. J. Neurophysiol. 79: 704–715, 1998. Saccade accuracy is known to be maintained by adaptive mechanisms that progressively reduce any visual error that consistently exists at the end of saccades. Experimentally, the visual error is induced using one of two paradigms. In the first, the horizontal and medial recti of trained monkeys are tenectomized and allowed to reattach so that both muscles are paretic. After patching the unoperated eye and forcing the monkey to use the “paretic eye,” saccades initially undershoot the intended target, but gradually increase in size until they almost acquire the target in one step. In the second, the target of a saccade is displaced in midsaccade so that the saccade cannot land on target. Again saccade size adapts until the target can be acquired in one step. Because adaptation with the latter paradigm is very rapid but adaptation using the former is slow, it has frequently been questioned whether or not the two forms of adaptation depend on the same neural mechanisms. We show that the rate of adaptation in both paradigms depends on the number of possible visual targets, so that when this variable is equated, adaptation occurs at similar rates in both paradigms. To demonstrate further similarities between the result of the two paradigms, an experiment using intrasaccadic displacements was conducted to show that rapid adaptation possesses the capacity to produce gain changes that vary with orbital position. The relative size of intrasaccadic displacements were graded with orbital position so as to mimic the position-dependent dysmetria initially produced by a single paretic extraocular muscle. Induced changes in saccade size paralleled the size of the displacements, being largest for saccades into one hemifield and being negligible for saccades into the other hemifield or in the opposite direction. Collectively, the data remove the rational for asserting that adaptation produced by the two paradigms depends on separate neural mechanisms. We argue that adaptation produced by both paradigms depends on the cerebellum.

A phrenic nerve-actuated electronically controlled positive-pressure ventilator

1987 ◽  
Vol 62 (5) ◽  
pp. 2121-2125 ◽  
Author(s):  
E. R. Schertel ◽  
D. A. Schneider ◽  
D. L. Howard ◽  
J. F. Green
Keyword(s):  
Moving Average ◽  
Inspiratory Flow ◽  
Positive Pressure ◽  
Feedback Signal ◽  
Position Signal ◽  
Tracheal Pressure ◽  
Valve Position ◽  
Air Valve ◽  
The Difference ◽  
Operational Modes

We have constructed an electronically controlled positive-pressure ventilator actuated by phrenic neural activity for use in open-chested or paralyzed experimental animals for the study of breathing pattern. A Bird Mark 14 positive-pressure ventilator was modified such that flow is a linear function of a command signal. Flow is delivered by advancing an air valve with a servo-motor that is controlled by one of three different operational modes. In two of the modes, the difference between the electronic average of inspiratory phrenic activity (moving average) and a feedback signal determines the inspiratory flow. The feedback signal is derived from either tracheal pressure or an electronic measure of inspired volume. In the third mode, the moving average is differentiated to provide control of inspiratory flow and volume. Physiological flow profiles were created using all three operational modes. Integration of an air-valve position signal provides an electronic measure of tidal volume. An additional feature of this ventilator allows inspiratory flow and duration to be predetermined for a given breath.

Baroreflex modulation of heart rate and initiation of atrial activation in dogs

1988 ◽  
Vol 255 (3) ◽  
pp. H503-H513 ◽  
Author(s):  
R. B. Schuessler ◽  
T. E. Canavan ◽  
J. P. Boineau ◽  
J. L. Cox
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Right Atrial ◽  
Autonomic Blockade ◽  
Left And Right ◽  
Atrial Activation ◽  
The Right ◽  
A Site ◽  
Induced Changes ◽  
Cardiac Nerves

In open-chest dogs, blood pressure was regulated by titrating doses of phenylephrine and nitroprusside to determine its effect on heart rate and pacemaker location. Changes in blood pressure correlated with changes in heart rate (r = 0.86). Activation time mapping demonstrated multicentric atrial activation, with a site of origin-rate relationship. The fastest pacemakers were located in the most cranial regions and slowest in the most caudal areas. In this chloralose-morphine anesthetized model, autonomic blockade with atropine and propranolol suggests that acute baroreflex-induced changes in heart rate were mediated exclusively by either increased sympathetic or parasympathetic tone and were not associated with inhibition of the opposite system. Division of right and left thoracic cardiac nerves indicated the left sympathetics participated in the baroreflex in 50% of the animals and the left parasympathetics in 90% of the animals. Both the right sympathetics and parasympathetics were active in the baroreflex in all animals. The data demonstrate that physiological heart rate response is regulated through an extensive system of right atrial pacemakers modulated by both left and right efferent cardiac nerves.

Three-Dimensional Ocular Kinematics During Eccentric Rotations: Evidence for Functional Rather Than Mechanical Constraints

2003 ◽  
Vol 89 (5) ◽  
pp. 2685-2696 ◽  
Author(s):  
Dora E. Angelaki
Keyword(s):  
Extraocular Muscle ◽  
Three Dimensional ◽  
Peripheral Retina ◽  
Eye Position ◽  
Image Stabilization ◽  
3D Kinematics ◽  
Mechanical Constraints ◽  
Rotation Axes ◽  
A Site ◽  
Eye Velocity

Previous studies have reported that the translational vestibuloocular reflex (TVOR) follows a three-dimensional (3D) kinematic behavior that is more similar to visually guided eye movements, like pursuit, rather than the rotational VOR (RVOR). Accordingly, TVOR rotation axes tilted with eye position toward an eye-fixed reference frame rather than staying relatively fixed in the head like in the RVOR. This difference arises because, contrary to the RVOR where peripheral image stability is functionally important, the TVOR like pursuit and saccades cares to stabilize images on the fovea. During most natural head and body movements, both VORs are simultaneously activated. In the present study, we have investigated in rhesus monkeys the 3D kinematics of the combined VOR during yaw rotation about eccentric axes. The experiments were motivated by and quantitatively compared with the predictions of two distinct hypotheses. According to the first (fixed-rule) hypothesis, an eye-position-dependent torsion is computed downstream of a site for RVOR/TVOR convergence, and the combined VOR axis would tilt through an angle that is proportional to gaze angle and independent of the relative RVOR/TVOR contributions to the total eye movement. This hypothesis would be consistent with the recently postulated mechanical constraints imposed by extraocular muscle pulleys. According to the second (image-stabilization) hypothesis, an eye-position-dependent torsion is computed separately for the RVOR and the TVOR components, implying a processing that takes place upstream of a site for RVOR/TVOR convergence. The latter hypothesis is based on the functional requirement that the 3D kinematics of the combined VOR should be governed by the need to keep images stable on the fovea with slip on the peripheral retina being dependent on the different functional goals of the two VORs. In contrast to the fixed-rule hypothesis, the data demonstrated a variable eye-position-dependent torsion for the combined VOR that was different for synergistic versus antagonistic RVOR/TVOR interactions. Furthermore, not only were the eye-velocity tilt slopes of the combined VOR as much as 10 times larger than what would be expected based on extraocular muscle pulley location, but also eye velocity during antagonistic RVOR/TVOR combinations often tilted opposite to gaze. These results are qualitatively and quantitatively consistent with the image-stabilization hypothesis, suggesting that the eye-position-dependent torsion is computed separately for the RVOR and the TVOR and that the 3D kinematics of the combined VOR are dependent on functional rather than mechanical constraints.

Postsaccadic eye position contributes to oculomotor error estimation in saccadic adaptation

2019 ◽  
Vol 122 (5) ◽  
pp. 1909-1917
Author(s):  
Svenja Gremmler ◽  
Markus Lappe
Keyword(s):  
Visual Feedback ◽  
Eye Position ◽  
Time Interval ◽  
Proprioceptive Information ◽  
Experimental Conditions ◽  
Position Information ◽  
Saccadic Adaptation ◽  
Position Signal ◽  
Motor Error ◽  
Saccade Control

We investigated whether the proprioceptive eye position signal after the execution of a saccadic eye movement is used to estimate the accuracy of the movement. If so, saccadic adaptation, the mechanism that maintains saccade accuracy, could use this signal in a similar way as it uses visual feedback after the saccade. To manipulate the availability of the proprioceptive eye position signal we utilized the finding that proprioceptive eye position information builds up gradually after a saccade over a time interval comparable to typical saccade latencies. We confined the retention time of gaze at the saccade landing point by asking participants to make fast return saccades to the fixation point that preempt the usability of proprioceptive eye position signals. In five experimental conditions we measured the influence of the visual and proprioceptive feedback, together and separately, on the development of adaptation. We found that the adaptation of the previously shortened saccades in the case of visual feedback being unavailable after the saccade was significantly weaker when the use of proprioceptive eye position information was impaired by fast return saccades. We conclude that adaptation can be driven by proprioceptive eye position feedback. NEW & NOTEWORTHY We show that proprioceptive eye position information is used after a saccade to estimate motor error and adapt saccade control. Previous studies on saccadic adaptation focused on visual feedback about saccade accuracy. A multimodal error signal combining visual and proprioceptive information is likely more robust. Moreover, combining proprioceptive and visual measures of saccade performance can be helpful to keep vision, proprioception, and motor control in alignment and produce a coherent representation of space.

On the Role of Calpain and Rho Proteins in Regulating Integrin-induced Signaling

1999 ◽  
Vol 82 (08) ◽  
pp. 385-391 ◽  
Author(s):  
Joan Fox
Keyword(s):  
Signaling Molecules ◽  
Cytoskeletal Proteins ◽  
Adherent Cells ◽  
Rho Proteins ◽  
Ligand Interactions ◽  
Platelet Aggregate ◽  
And Migration ◽  
Key Steps ◽  
A Site ◽  
Induced Changes

SummaryThe integrin family of transmembrane receptors plays an essential role in inducing the adhesion of cells to the extracellular matrix. In some cases, members of this family of receptors can bind soluble ligands or can bind receptors on other cells and, in this way, mediate interactions between cells. In all cases, once an integrin has bound, ligand signals are transmitted across the occupied integrin. These signals culminate in changes in the behavior of the cell appropriate for the adherent state of the cell. For example, in the case of platelets, an end result of the signaling induced by binding of fibrinogen to αIIbβ3 in a platelet aggregate is a reorganization of the cytoskeleton that leads to retraction of externally-bound fibrin by clots.1,2 In the case of neutrophils, cytoskeletal changes following the integrininduced interaction of neutrophils with endothelial cells lead to the migration of neutrophils into a site of injury.3,4 Other examples of the consequences of integrin-induced signaling in adherent cells include the trafficking of lymphocytes and migration of cells during development, angiogenesis, and metastasis.5-7 Numerous signaling molecules have been shown to be activated following integrin-ligand interactions.8 Many of these associate in complexes with ligand-occupied integrin and cytoskeletal proteins. However, in general, little is known about the key steps involved regarding integrin-induced changes in the behavior of adherent cells. The present chapter reviews steps involved in integrin-induced signaling, describes the evidence that calpain is one of the signaling molecules involved in this signal transduction, and discusses potential mechanisms by which cleavage of cytoskeletal proteins and signaling molecules by calpain may regulate the integrin-induced changes in cell behavior.

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