scholarly journals The Response of MSTd Neurons to Perturbations in Target Motion During Ongoing Smooth-Pursuit Eye Movements

2010 ◽  
Vol 103 (1) ◽  
pp. 519-530 ◽  
Author(s):  
Seiji Ono ◽  
Lukas Brostek ◽  
Ulrich Nuding ◽  
Stefan Glasauer ◽  
Ulrich Büttner ◽  
...  
Keyword(s):  
Eye Movement ◽  
Smooth Pursuit ◽  
Dynamic Properties ◽  
Receptive Fields ◽  
Gain Control ◽  
Frontal Eye Field ◽  
Cortical Areas ◽  
Target Perturbation ◽  
Behaving Monkeys ◽  
Dynamic Gain

Several regions of the brain are involved in smooth-pursuit eye movement (SPEM) control, including the cortical areas MST (medial superior temporal) and FEF (frontal eye field). It has been shown that the eye-movement responses to a brief perturbation of the visual target during ongoing pursuit increases with higher pursuit velocities. To further investigate the underlying neuronal mechanism of this nonlinear dynamic gain control and the contributions of different cortical areas to it, we recorded from MSTd (dorsal division of the MST area) neurons in behaving monkeys ( Macaca mulatta) during step-ramp SPEM (5–20°/s) with and without superimposed target perturbation (one cycle, 5 Hz, ±10°/s). Smooth-pursuit–related MSTd neurons started to increase their activity on average 127 ms after eye-movement onset. Target perturbation consistently led to larger eye-movement responses and decreasing latencies with increasing ramp velocities, as predicted by dynamic gain control. For 36% of the smooth-pursuit–related MSTd neurons the eye-movement perturbation was accompanied by detectable changes in neuronal activity with a latency of 102 ms, with respect to the eye-movement response. The remaining smooth-pursuit–related MSTd neurons (64%) did not reflect the eye-movement perturbation. For the large majority of cases this finding could be predicted by the dynamic properties of the step-ramp responses. Almost all these MSTd neurons had large visual receptive fields responding to motion in preferred directions opposite to the optimal SPEM stimulus. Based on these findings it is unlikely that MSTd plays a major role for dynamic gain control and initiation of the perturbation response. However, neurons in MSTd could still participate in SPEM maintenance. Due to their visual field properties they could also play a role in other functions such as self-motion perception.

scholarly journals A Theory of the Dual Pathways for Smooth Pursuit Based on Dynamic Gain Control

2008 ◽  
Vol 99 (6) ◽  
pp. 2798-2808 ◽  
Author(s):  
Ulrich Nuding ◽  
Seiji Ono ◽  
Michael J. Mustari ◽  
Ulrich Büttner ◽  
Stefan Glasauer
Keyword(s):  
Brain Stem ◽  
Smooth Pursuit ◽  
Gain Control ◽  
Salient Feature ◽  
Target Motion ◽  
Temporal Area ◽  
Parallel Pathways ◽  
Medial Superior Temporal ◽  
Behavioral Paradigm ◽  
Dynamic Gain

The smooth pursuit eye movement (SPEM) system is much more sensitive to target motion perturbations during pursuit than during fixation. This sensitivity is commonly attributed to a dynamic gain control mechanism. Neither the neural substrate nor the functional architecture for this gain control has been fully revealed. There are at least two cortical areas that crucially contribute to smooth pursuit and are therefore eligible sites for dynamic gain control: the medial superior temporal area (MST) and the pursuit area of the frontal eye fields (FEFs), which both project to brain stem premotor structures via parallel pathways. The aim of this study was to develop a model of smooth pursuit based on behavioral, anatomical, and neurophysiological results to account for nonlinear dynamic gain control. Using a behavioral paradigm in humans consisting of a sinusoidal oscillation (4 Hz, ±8°/s) superimposed on a constant velocity target motion (0–24°/s), we were able to identify relevant gain control parameters in the model. A salient feature of our model is the emergence of two parallel pathways from higher visual cortical to lower motor areas in the brain stem that correspond to the MST and FEF pathways. Detailed analysis of the model revealed that one pathway mainly carries eye velocity related signals, whereas the other is associated mostly with eye acceleration. From comparison with known neurophysiological results we conclude that the dynamic gain control can be attributed to the FEF pathway, whereas the MST pathway serves as the basic circuit for maintaining an ongoing SPEM.

scholarly journals Deficits in Smooth-Pursuit Eye Movements After Muscimol Inactivation Within the Primate's Frontal Eye Field

1998 ◽  
Vol 80 (1) ◽  
pp. 458-464 ◽  
Author(s):  
Dexiu Shi ◽  
Harriet R. Friedman ◽  
Charles J. Bruce
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Smooth Pursuit ◽  
Critical Factor ◽  
Movement Direction ◽  
Frontal Eye Field ◽  
Smooth Pursuit Eye Movements ◽  
Motion Onset ◽  
Pursuit Eye Movements ◽  
Eye Field

Shi, Dexiu, Harriet R. Friedman, and Charles J. Bruce. Deficits in smooth-pursuit eye movements after muscimol inactivation within the primate's frontal eye field. J. Neurophysiol. 80: 458–464, 1998. To evaluate smooth-pursuit (SP) function in the primate frontal eye field (FEF), microinjections of muscimol, a γ-aminobutyric acid (GABA) agonist, were used to reversibly deactivate physiologically characterized sites in FEF. SP was severely impaired by deactivation at sites in the FEF's smooth eye movement region (FEFsem) located in the fundus and posterior bank of the macaque monkey's arcuate sulcus. These SP deficits were apparent immediately after the muscimol injection and persisted for several hours but recovered by the next day. SP was most drastically and consistently impaired for directions similar to the injected site's elicited smooth eye movement direction or to the optimal SP direction for its neuronal responses. Targets moving in these directions, usually ipsilateral to the injected hemisphere, were tracked primarily with saccades after the muscimol injection, the peak SP velocity being only 10–30% of preinjection velocity. SP in other directions, including contralateral, was less strongly affected. Initial SP acceleration in response to target motion onset was also significantly diminished, generally by approximately the same proportion as peak SP velocity. In contrast, saccades were largely unaffected by muscimol injections in FEFsem; nor was there an immediate effect on SP when control sites in the saccadic region of FEF (FEFsac) were deactivated, although a SP deficit often appeared 30–60 min after FEFsac injections, possibly reflecting diffusion of muscimol into neighboring FEFsem. These reversible SP deficits produced by muscimol inactivation within FEFsem are similar to permanent deficits caused by large aspiration lesions of FEF and indicate that inclusion of FEFsem is the critical factor determining whether FEF lesions impair SP. The severity of the reversible deficits found here indicates how extremely critical FEFsem is for normal highgain SP.

scholarly journals Suppression of frontal eye field neuronal responses with maintained fixation

2018 ◽  
Vol 115 (4) ◽  
pp. 804-809 ◽  
Author(s):  
Koorosh Mirpour ◽  
Zeinab Bolandnazar ◽  
James W. Bisley
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Scene Perception ◽  
Receptive Fields ◽  
Movement Behavior ◽  
Frontal Eye Field ◽  
Neuronal Responses ◽  
Eye Field ◽  
Foraging Task ◽  
Temporal Flow

The decision of where to make an eye movement is thought to be driven primarily by responses to stimuli in neurons’ receptive fields (RFs) in oculomotor areas, including the frontal eye field (FEF) of prefrontal cortex. It is also thought that a saccade may be generated when the accumulation of this activity in favor of one location or another reaches a threshold. However, in the reading and scene perception fields, it is well known that the properties of the stimulus at the fovea often affect when the eyes leave that stimulus. We propose that if FEF plays a role in generating eye movements, then the identity of the stimulus at fixation should affect the FEF responses so as to reduce the probability of making a saccade when fixating an item of interest. Using a visual foraging task in which animals could make multiple eye movements within a single trial, we found that responses were strongly modulated by the identity of the stimulus at the fovea. Specifically, responses to the stimulus in the RF were suppressed when the animal maintained fixation for longer durations on a stimulus that could be associated with a reward. We suggest that this suppression, which was predicted by models of eye movement behavior, could be a mechanism by which FEF can modulate the temporal flow of saccades based on the importance of the stimulus at the fovea.

scholarly journals Alterations of Eye Movement Control in Neurodegenerative Movement Disorders

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Martin Gorges ◽  
Elmar H. Pinkhardt ◽  
Jan Kassubek
Keyword(s):  
Basal Ganglia ◽  
Eye Movement ◽  
Movement Disorders ◽  
Smooth Pursuit ◽  
Movement Control ◽  
Pathological Process ◽  
Functional Deficits ◽  
Cortical Areas ◽  
Oculomotor Nuclei

The evolution of the fovea centralis, the most central part of the retina and the area of the highest visual accuracy, requires humans to shift their gaze rapidly (saccades) to bring some object of interest within the visual field onto the fovea. In addition, humans are equipped with the ability to rotate the eye ball continuously in a highly predicting manner (smooth pursuit) to hold a moving target steadily upon the retina. The functional deficits in neurodegenerative movement disorders (e.g., Parkinsonian syndromes) involve the basal ganglia that are critical in all aspects of movement control. Moreover, neocortical structures, the cerebellum, and the midbrain may become affected by the pathological process. A broad spectrum of eye movement alterations may result, comprising smooth pursuit disturbance (e.g., interrupting saccades), saccadic dysfunction (e.g., hypometric saccades), and abnormal attempted fixation (e.g., pathological nystagmus and square wave jerks). On clinical grounds, videooculography is a sensitive noninvasivein vivotechnique to classify oculomotion function alterations. Eye movements are a valuable window into the integrity of central nervous system structures and their changes in defined neurodegenerative conditions, that is, the oculomotor nuclei in the brainstem together with their directly activating supranuclear centers and the basal ganglia as well as cortical areas of higher cognitive control of attention.

A bang-bang PLL employing dynamic gain control for low jitter and fast lock times

2006 ◽  
Vol 49 (2) ◽  
pp. 131-140 ◽  
Author(s):  
Michael J. Chan ◽  
Adam Postula ◽  
Yong Ding ◽  
Lech Jozwiak
Keyword(s):  
Gain Control ◽  
Low Jitter ◽  
Dynamic Gain

scholarly journals Role of Primate Cerebellar Hemisphere in Voluntary Eye Movement Control Revealed by Lesion Effects

2009 ◽  
Vol 101 (2) ◽  
pp. 934-947 ◽  
Author(s):  
Masafumi Ohki ◽  
Hiromasa Kitazawa ◽  
Takahito Hiramatsu ◽  
Kimitake Kaga ◽  
Taiko Kitamura ◽  
...  
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Smooth Pursuit ◽  
Movement Control ◽  
Cerebellar Hemisphere ◽  
Target Velocity ◽  
Eye Movement Control ◽  
Pursuit Eye Movements ◽  
Catch Up

The anatomical connection between the frontal eye field and the cerebellar hemispheric lobule VII (H-VII) suggests a potential role of the hemisphere in voluntary eye movement control. To reveal the involvement of the hemisphere in smooth pursuit and saccade control, we made a unilateral lesion around H-VII and examined its effects in three Macaca fuscata that were trained to pursue visually a small target. To the step (3°)-ramp (5–20°/s) target motion, the monkeys usually showed an initial pursuit eye movement at a latency of 80–140 ms and a small catch-up saccade at 140–220 ms that was followed by a postsaccadic pursuit eye movement that roughly matched the ramp target velocity. After unilateral cerebellar hemispheric lesioning, the initial pursuit eye movements were impaired, and the velocities of the postsaccadic pursuit eye movements decreased. The onsets of 5° visually guided saccades to the stationary target were delayed, and their amplitudes showed a tendency of increased trial-to-trial variability but never became hypo- or hypermetric. Similar tendencies were observed in the onsets and amplitudes of catch-up saccades. The adaptation of open-loop smooth pursuit velocity, tested by a step increase in target velocity for a brief period, was impaired. These lesion effects were recognized in all directions, particularly in the ipsiversive direction. A recovery was observed at 4 wk postlesion for some of these lesion effects. These results suggest that the cerebellar hemispheric region around lobule VII is involved in the control of smooth pursuit and saccadic eye movements.

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