Role of cat pontine burst neurons in generation of saccadic eye movements.

1981 ◽  
Vol 46 (3) ◽  
pp. 387-408 ◽  
Author(s):  
C R Kaneko ◽  
C Evinger ◽  
A F Fuchs
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
David Melcher ◽  
Devpriya Kumar ◽  
Narayanan Srinivasan

Abstract Visual perception is based on periods of stable fixation separated by saccadic eye movements. Although naive perception seems stable (in space) and continuous (in time), laboratory studies have demonstrated that events presented around the time of saccades are misperceived spatially and temporally. Saccadic chronostasis, the “stopped clock illusion”, represents one such temporal distortion in which the movement of the clock hand after the saccade is perceived as lasting longer than usual. Multiple explanations for chronostasis have been proposed including action-backdating, temporal binding of the action towards the moment of its effect (“intentional binding”) and post-saccadic temporal dilation. The current study aimed to resolve this debate by using different types of action (keypress vs saccade) and varying the intentionality of the action. We measured both perceived onset of the motor action and perceived onset of an auditory tone presented at different delays after the keypress/saccade. The results showed intentional binding for the keypress action, with perceived motor onset shifted forwards in time and the time of the tone shifted backwards. Saccades resulted in the opposite pattern, showing temporal expansion rather than compression, especially with cued saccades. The temporal illusion was modulated by intentionality of the movement. Our findings suggest that saccadic chronostasis is not solely dependent on a backward shift in perceived saccade onset, but instead reflects a temporal dilation. This percept of an effectively “longer” period at the beginning of a new fixation may reflect the pattern of suppressed, and then enhanced, visual processing around the time of saccades.


2019 ◽  
Vol 237 (11) ◽  
pp. 3033-3045
Author(s):  
Eugene McSorley ◽  
Iain D. Gilchrist ◽  
Rachel McCloy

Abstract One of the core mechanisms involved in the control of saccade responses to selected target stimuli is the disengagement from the current fixation location, so that the next saccade can be executed. To carry out everyday visual tasks, we make multiple eye movements that can be programmed in parallel. However, the role of disengagement in the parallel programming of saccades has not been examined. It is well established that the need for disengagement slows down saccadic response time. This may be important in allowing the system to program accurate eye movements and have a role to play in the control of multiple eye movements but as yet this remains untested. Here, we report two experiments that seek to examine whether fixation disengagement reduces saccade latencies when the task completion demands multiple saccade responses. A saccade contingent paradigm was employed and participants were asked to execute saccadic eye movements to a series of seven targets while manipulating when these targets were shown. This both promotes fixation disengagement and controls the extent that parallel programming can occur. We found that trial duration decreased as more targets were made available prior to fixation: this was a result both of a reduction in the number of saccades being executed and in their saccade latencies. This supports the view that even when fixation disengagement is not required, parallel programming of multiple sequential saccadic eye movements is still present. By comparison with previous published data, we demonstrate a substantial speeded of response times in these condition (“a gap effect”) and that parallel programming is attenuated in these conditions.


2006 ◽  
Vol 95 (2) ◽  
pp. 979-994 ◽  
Author(s):  
Chris R. S. Kaneko

The paramedian pontine reticular formation contains the premotoneuronal cell groups that constitute the saccadic burst generator and control saccadic eye movements. Despite years of study and numerous investigations, the rostral portion of this area has received comparatively little attention, particularly the cell type known as long-lead burst neurons (LLBNs). Several hypotheses about the functional role of LLBNs in saccade generation have been proposed, although there is little information with which to assess them. To address this issue, I mapped and recorded LLBNs in the rostral pons to measure their discharge characteristics and correlate those characteristics with the metrics of the concurrent saccades. On the basis of their discharge and location, I identified three types of LLBNs in the rostral pons: excitatory (eLLBN), dorsal (dLLBN), and nucleus reticularis tegmenti pontis (nrtp) LLBNs. The eLLBNs, encountered throughout the pons, discharge for ipsilateral saccades in proportion to saccade amplitude, velocity, and duration. The dLLBNs, found at the pontomesencephalic junction, discharge maximally for ipsilateral saccades of a particular amplitude, usually <10°, and are not associated with a particular anatomical nucleus. The nrtp LLBNs, previously described as vector LLBNs, discharge for saccades of a particular direction and sometimes a particular amplitude. The discharge of the eLLBNs suggests they drive motor neurons. The anatomical projections of the nrtp LLBNs suggest that their involvement in saccade production is less direct. The discharge of dLLBNs is consistent with a role in providing the “trigger” signal that initiates saccades.


2009 ◽  
Vol 147 (1) ◽  
pp. 11-14
Author(s):  
N. A. Ryabchikova ◽  
B. H. Bazyian ◽  
V. B. Poliansky ◽  
O. A. Pletnev

2008 ◽  
Vol 119 (9) ◽  
pp. e166
Author(s):  
S.L. Gonzalez Andino ◽  
C. Laine ◽  
R. Grave de Peralta ◽  
K.L. Gothard

1998 ◽  
Vol 119 (1) ◽  
pp. 49-54 ◽  
Author(s):  
Susan J. Herdman

Recovery of gaze and postural stability in human beings with vestibular deficits is well documented. The mechanisms that contribute to this recovery form the basis for the exercises used in the rehabilitation of these patients. These mechanisms include the central preprogramming of eye movements and of postural responses, the potentiation of the cervico-ocular reflex, modification of saccadic eye movements, and the substitution of visual and somatosensory cues for the lost vestibular cues. The mechanism most successful in contributing to recovery, however, is probably adaptation of the vestibular system itself. Understanding the various compensatory mechanisms and their limitations for improving gaze and postural stability should lead to more effective treatment of these patients. (Otolaryngol Head Neck Surg 1998;119:49–54.)


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