scholarly journals Short-latency allocentric control of saccadic eye movements

2017 ◽  
Vol 117 (1) ◽  
pp. 376-387 ◽  
Author(s):  
Mrinmoy Chakrabarty ◽  
Tamami Nakano ◽  
Shigeru Kitazawa

It is generally accepted that the neural circuits that are implicated in saccade control use retinotopically coded target locations. However, several studies have revealed that nonretinotopic representation is also used. This idea raises a question about whether nonretinotopic coding is egocentric (head or body centered) or allocentric (environment centered). In the current study, we hypothesized that allocentric coding may play a crucial role in immediate saccade control. To test this hypothesis, we used an immediate double-step saccade task toward two sequentially flashed targets with a frame in the background, and we examined whether the end point of the second saccade was affected by a transient shift of the background that participants were told to ignore. When the background was shifted transiently upward (or downward) during the flash of the second target, the second saccade generally erred the target downward (or upward), which was in the direction opposite to the shift of the background. The effect on the second saccade became significant within 150 ms after the frame was presented for decoding and was built up for 200 ms thereafter. When the second saccade was not adjusted, a small, corrective saccade followed within 300 ms. The effect scaled linearly with the shift size up to 3° for a noncorrective second saccade and up to 6° for a corrective saccade. The present results show that an allocentric location of a target is rapidly represented by the brain and used for controlling saccades. NEW & NOTEWORTHY We found that the saccade end point was shifted from the actual target position toward the direction expected from allocentric coding when a large frame in the background was transiently shifted during the period of target presentation. The effect occurred within 150 ms. The present study provides direct evidence that the brain rapidly uses allocentric coding of a target to control immediate saccades.

2007 ◽  
Vol 19 (9) ◽  
pp. 2353-2386 ◽  
Author(s):  
Carlos R. Cassanello ◽  
Vincent P. Ferrera

Saccadic eye movements remain spatially accurate even when the target becomes invisible and the initial eye position is perturbed. The brain accomplishes this in part by remapping the remembered target location in retinal coordinates. The computation that underlies this visual remapping is approximated by vector subtraction: the original saccade vector is updated by subtracting the vector corresponding to the intervening eye movement. The neural mechanism by which vector subtraction is implemented is not fully understood. Here, we investigate vector subtraction within a framework in which eye position and retinal target position signals interact multiplicatively (gain field). When the eyes move, they induce a spatial modulation of the firing rates across a retinotopic map of neurons. The updated saccade metric can be read from the shift of the peak of the population activity across the map. This model uses a quasi-linear (half-rectified) dependence on the eye position and requires the slope of the eye position input to be negatively proportional to the preferred retinal position of each neuron. We derive analytically this constraint and study its range of validity. We discuss how this mechanism relates to experimental results reported in the frontal eye fields of macaque monkeys.


2013 ◽  
Vol 110 (4) ◽  
pp. 807-816 ◽  
Author(s):  
Brandie M. Stewart ◽  
Lee A. Baugh ◽  
Jason P. Gallivan ◽  
J. Randall Flanagan

Reaches performed in many natural situations involve selecting a specific target from a number of alternatives. Recent studies show that before reaching, multiple potential reach targets are encoded in brain regions involved in action control and that, when people are required to initiate the reach before the target is specified, initial hand direction is biased by the spatial distribution of potential targets. These findings have led to the suggestion that the brain, during planning, simultaneously prepares multiple reaches to potential targets. In addition to hand direction, reach planning often involves specifying other parameters such as wrist orientation. For example, when posting a letter in a mail slot, both the location and orientation of the slot must be encoded to control hand direction and orientation. Therefore, if the brain prepares multiple reaches to potential targets and if these targets require the specification of hand direction and orientation, then both of these variables should be biased by the spatial distribution of potential targets. To test this prediction, we examined a task in which participants moved a hand-held rectangular tool toward multiple rectangular targets of varying location and orientation, one of which was selected, with equal probability as the actual target after movement initiation. We found that initial hand direction and orientation were biased by the spatial distributions of potential target locations and orientations, respectively. This result is consistent with the idea that the brain, in cases of target uncertainty, simultaneously plans fully specified reaching movements to all potential targets.


2006 ◽  
Vol 95 (6) ◽  
pp. 3502-3511 ◽  
Author(s):  
C. Kip Rodgers ◽  
Douglas P. Munoz ◽  
Stephen H. Scott ◽  
Martin Paré

The intermediate layers of the superior colliculus (SC) contain neurons that clearly play a major role in regulating the production of saccadic eye movements: a burst of activity from saccade neurons (SNs) is thought to provide a drive signal to set the eyes in motion, whereas the tonic activity of fixation neurons (FNs) is thought to suppress saccades during fixation. The exact contribution of these neurons to saccade control is, however, unclear because the nature of the signals sent by the SC to the brain stem saccade generation circuit has not been studied in detail. Here we tested the hypothesis that the SC output signal is sufficient to control saccades by examining whether antidromically identified tectoreticular neurons (TRNs: 33 SNs and 13 FNs) determine the end of saccades. First, TRNs had discharge properties similar to those of nonidentified SC neurons and a proportion of output SNs had visually evoked responses, which signify that the saccade generator must receive and process visual information. Second, only a minority of TRNs possessed the temporal patterns of activity sufficient to terminate saccades: Output SNs did not cease discharging at the time of saccade end, possibly continuing to drive the brain stem during postsaccadic fixations, and output FNs did not resume their activity before saccade end. These results argue against a role for SC in regulating the timing of saccade termination by a temporal code and suggest that other saccade centers act to thwart the extraneous SC drive signal, unless it controls saccade termination by a spatial code.


2009 ◽  
Vol 101 (1) ◽  
pp. 448-459 ◽  
Author(s):  
Michael Campos ◽  
Boris Breznen ◽  
Richard A. Andersen

When different stimuli indicate where and when to make an eye movement, the brain areas involved in oculomotor control must selectively plan an eye movement to the stimulus that encodes the target position and also encode the information available from the timing cue. This could pose a challenge to the oculomotor system since the representation of the timing stimulus location in one brain area might be interpreted by downstream neurons as a competing motor plan. Evidence from diverse sources has suggested that the supplementary eye fields (SEF) play an important role in behavioral timing, so we recorded single-unit activity from SEF to characterize how target and timing cues are encoded in this region. Two monkeys performed a variant of the memory-guided saccade task, in which a timing stimulus was presented at a randomly chosen eccentric location. Many spatially tuned SEF neurons encoded only the location of the target and not the timing stimulus, whereas several other SEF neurons encoded the location of the timing stimulus and not the target. The SEF population therefore encoded the location of each stimulus with largely distinct neuronal subpopulations. For comparison, we recorded a small population of lateral intraparietal (LIP) neurons in the same task. We found that most LIP neurons that encoded the location of the target also encoded the location of the timing stimulus after its presentation, but selectively encoded the intended eye movement plan in advance of saccade initiation. These results suggest that SEF, by conditionally encoding the location of instructional stimuli depending on their meaning, can help identify which movement plan represented in other oculomotor structures, such as LIP, should be selected for the next eye movement.


2007 ◽  
Vol 98 (6) ◽  
pp. 3163-3170 ◽  
Author(s):  
Takuro Ikeda ◽  
Okihide Hikosaka

Expectation of reward is crucial for goal-directed behavior of animals. However, little is known about how reward information is used in the brain at the time of action. We investigated this question by recording from single neurons in the macaque superior colliculus (SC) while the animal was performing a memory-guided saccade task with an asymmetrical reward schedule. The SC is an ideal structure to ask this question because it receives inputs from many brain areas including the prefrontal cortex and the basal ganglia where reward information is thought to be encoded and sends motor commands to the brain stem saccade generators. We found two groups of SC neurons that encoded reward information in the presaccadic period: positive reward-coding neurons that showed higher activity when reward was expected and negative reward-coding neurons that showed higher activity when reward was not expected. The positive reward-coding usually started even before a cue for target position was presented, whereas the negative reward-coding was largely restricted to the presaccadic period. The two kinds of reward-coding may be useful for the animal to select an appropriate behavior in a complex environment.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
O.V Petyunina ◽  
M.P Kopytsya ◽  
A.E Berezin ◽  
A.A Berezin

Abstract Background The single nucleotide polymorphism (SNP) Val66Met (rs6265) of the brain-derived neurotrophic factor (BDNF) gene is a possible candidate that is associated with the development of psychopathology and combines it with cardiovascular events. Purpose To research the possible associations of single-nucleotide polymorphism of Val66Met BDNF gene with the occurrence of endpoints after 6 months of follow-up after ST segment elevation myocardial infarction (STEMI). Methods 256 acute STEMI patients after successful primary percutaneous coronary intervention (PCI) were enrolled in the study. TIMI III blood flow restoring through culprit artery was determined. The study of SNP of Val66Met (rs6265) of the BDNF gene was performed by real-time polymerase chain reaction. The emotional state of the patients and its relationship with stress were assessed with the questionnaire “Depression, Anxiety and Stress-21”. All acute STEMI patients received adjuvant treatment due to current ESC recommendations. All procedures performed in the study involving human participants were in accordance with the ethical standards and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards and approved by the local ethics committee. Written inform consent was obtained from each patient. The primary endpoint was combined event (follow-up major adverse cardiac events – MACEs and hospitalization) that occurred within 6-month of the discharge from the hospital. MACEs were defined as the composite of CV death, recurrent angina, newly diagnosed heart failure. Results The frequency of genotypes Val66Met gene for BDNF in STEMI patients (n=256) was the following: 66ValVal=74.2% (n=190), 66ValMet + 66MetMet – 25.8% (n=66). The 66ValMet + 66MetMet polymorphism in the BDNF gene, stress and anxiety on 10–14 days before the event, as well as reduced left ventricular ejection fraction (LVEF), were independently associated with combined 6 months clinical end point after STEMI. Severity of depression according to depression scale was more profound in individuals with 66ValMet+66MetMet polymorphysms in BDNF gene (P=0.045) than in patients with 66ValVal genotype. Univariate and multivariate linear regressions has shown that 66ValMet+66MetMet genotype in BDNF gene, anxiety and stress before event, LVEF had independent power on dependent variable entitled combined end point after 6 month observation for STEMI patients with successful revascularization (P=0.0395). Kaplan-Meier curves demonstrated that STEMI patients with 66ValVal genotype in BDNF gene had a lower accumulation of combined end point compared with acute STEMI patients with 66ValMet+66ValMet polymorphism (Cox-criterion, P=0.019; log-rang criterion, P=0.03). Conclusion The Val66Met polymorphism in BDNF gene was found as an independent predictor for combined 6-month clinical end points after acute STEMI treated primary PCI. Funding Acknowledgement Type of funding source: None


2013 ◽  
Vol 109 (2) ◽  
pp. 518-545 ◽  
Author(s):  
K. P. Schultz ◽  
C. Busettini

Saccadic eye movements are rapid transfers of gaze between objects of interest. Their duration is too short for the visual system to be able to follow their progress in time. Adaptive mechanisms constantly recalibrate the saccadic responses by detecting how close the landings are to the selected targets. The double-step saccadic paradigm is a common method to simulate alterations in saccadic gain. While the subject is responding to a first target shift, a second shift is introduced in the middle of this movement, which masks it from visual detection. The error in landing introduced by the second shift is interpreted by the brain as an error in the programming of the initial response, with gradual gain changes aimed at compensating the apparent sensorimotor mismatch. A second shift applied dichoptically to only one eye introduces disconjugate landing errors between the two eyes. A monocular adaptive system would independently modify only the gain of the eye exposed to the second shift in order to reestablish binocular alignment. Our results support a binocular mechanism. A version-based saccadic adaptive process detects postsaccadic version errors and generates compensatory conjugate gain alterations. A vergence-based saccadic adaptive process detects postsaccadic disparity errors and generates corrective nonvisual disparity signals that are sent to the vergence system to regain binocularity. This results in striking dynamical similarities between visually driven combined saccade-vergence gaze transfers, where the disparity is given by the visual targets, and the double-step adaptive disconjugate responses, where an adaptive disparity signal is generated internally by the saccadic system.


1993 ◽  
Vol 70 (5) ◽  
pp. 1741-1758 ◽  
Author(s):  
F. R. Robinson ◽  
A. Straube ◽  
A. F. Fuchs

1. We studied the effect of temporarily inhibiting neurons in the caudal fastigial nucleus in two rhesus macaques trained to make saccades to jumping targets. We placed injections of the gamma-aminobutyric acid (GABA) agonist muscimol unilaterally or bilaterally at sites in the caudal fastigial nucleus where we had recorded saccade-related neurons a few minutes earlier. 2. Unilateral injections (n = 9) made horizontal saccades to the injected side hypermetric and those to the other side hypometric (mean gain of 1.37 and 0.61, respectively, for 10 degrees target steps, and 1.26 and 0.81 for 20 degrees target steps; normal saccade gain was 0.96). Saccades to vertical targets showed a small but significant hypermetria and curved strongly toward the side of the injection. The trajectories and end points of all targeted saccades were more variable than normal. 3. After unilateral injections, centripetal saccades were slightly larger than centrifugal saccades (mean gains for ipsilateral saccades were 1.42 and 1.31, respectively, for 10 degrees target steps, and 1.37 and 1.15 for 20 degrees target steps). 4. Unilateral injections increased the average acceleration of ipsilateral saccades and decreased the acceleration of contralateral saccades. Injections decreased both the acceleration and deceleration of vertical saccades. 5. After dysmetric saccades, monkeys acquired the target with an abnormally high number of hypometric corrective saccades. Injection increased the average number of corrective saccades from 0.6 to 2.1 after 10 degrees horizontal target steps and from 0.8 to 2.1 after 20 degrees steps. The size of each successive corrective saccade in a series decreased, and the latency from the previous corrective saccade increased. 6. Bilateral injections (n = 2) of muscimol, in which we injected first into the left caudal fastigial nucleus and then, within 30 min, into the right, made all saccades hypermetric (mean gain for 10 degrees right, left, up, and down saccades was 1.18, 1.49, 1.43, and 1.10, respectively). Paradoxically, bilateral injection decreased both saccade acceleration and deceleration. Saccade trajectories and end points were more variable than normal. 7. To account for the effects of our injections, we propose that the activity of caudal fastigial neurons on one side normally helps to decelerate ipsilateral saccades and helps to accelerate contralateral saccades by influencing the feedback loop of the saccade burst generator in the brain stem. Without caudal fastigial activity the brain stem burst generator produces hypermetric, variable saccades. We therefore also propose that the influence of caudal fastigial neurons on the burst generator makes saccades more consistent and accurate.(ABSTRACT TRUNCATED AT 400 WORDS)


2008 ◽  
Vol 99 (5) ◽  
pp. 2602-2616 ◽  
Author(s):  
Marion R. Van Horn ◽  
Pierre A. Sylvestre ◽  
Kathleen E. Cullen

When we look between objects located at different depths the horizontal movement of each eye is different from that of the other, yet temporally synchronized. Traditionally, a vergence-specific neuronal subsystem, independent from other oculomotor subsystems, has been thought to generate all eye movements in depth. However, recent studies have challenged this view by unmasking interactions between vergence and saccadic eye movements during disconjugate saccades. Here, we combined experimental and modeling approaches to address whether the premotor command to generate disconjugate saccades originates exclusively in “vergence centers.” We found that the brain stem burst generator, which is commonly assumed to drive only the conjugate component of eye movements, carries substantial vergence-related information during disconjugate saccades. Notably, facilitated vergence velocities during disconjugate saccades were synchronized with the burst onset of excitatory and inhibitory brain stem saccadic burst neurons (SBNs). Furthermore, the time-varying discharge properties of the majority of SBNs (>70%) preferentially encoded the dynamics of an individual eye during disconjugate saccades. When these experimental results were implemented into a computer-based simulation, to further evaluate the contribution of the saccadic burst generator in generating disconjugate saccades, we found that it carries all the vergence drive that is necessary to shape the activity of the abducens motoneurons to which it projects. Taken together, our results provide evidence that the premotor commands from the brain stem saccadic circuitry, to the target motoneurons, are sufficient to ensure the accurate control shifts of gaze in three dimensions.


2019 ◽  
Author(s):  
Dirk van Moorselaar ◽  
Heleen A. Slagter

AbstractIt is well known that attention can facilitate performance by top-down biasing processing of task-relevant information in advance. Recent findings from behavioral studies suggest that distractor inhibition is not under similar direct control, but strongly dependent on expectations derived from previous experience. Yet, how expectations about distracting information influence distractor inhibition at the neural level remains unclear. The current study addressed this outstanding question in three experiments in which search displays with repeating distractor or target locations across trials allowed observers to learn which location to selectively suppress or boost. Behavioral findings demonstrated that both distractor and target location learning resulted in more efficient search, as indexed by faster response times. Crucially, benefits of distractor learning were observed without target location foreknowledge, unaffected by the number of possible target locations, and could not be explained by priming alone. To determine how distractor location expectations facilitated performance, we applied a spatial encoding model to EEG data to reconstruct activity in neural populations tuned to the distractor or target location. Target location learning increased neural tuning to the target location in advance, indicative of preparatory biasing. This sensitivity increased after target presentation. By contrast, distractor expectations did not change preparatory spatial tuning. Instead, distractor expectations reduced distractor-specific processing, as reflected in the disappearance of the Pd ERP component, a neural marker of distractor inhibition, and decreased decoding accuracy. These findings suggest that the brain may no longer process expected distractors as distractors, once it has learned they can safely be ignored.Significance statementWe constantly try hard to ignore conspicuous events that distract us from our current goals. Surprisingly, and in contrast to dominant attention theories, ignoring distracting, but irrelevant events does not seem to be as flexible as is focusing our attention on those same aspects. Instead, distractor suppression appears to strongly rely on learned, context-dependent expectations. Here, we investigated how learning about upcoming distractors changes distractor processing and directly contrasted the underlying neural dynamics to target learning. We show that while target learning enhanced anticipatory sensory tuning, distractor learning only modulated reactive suppressive processing. These results suggest that expected distractors may no longer be considered distractors by the brain once it has learned that they can safely be ignored.


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