A quantitative analysis of generation of saccadic eye movements by burst neurons

Gisbergen, J.A.M. van; Robinson, David A.; Gielen, Stan

doi:10.1152/jn.1981.45.3.417

Cited by 589 publications

(380 citation statements)

References 14 publications

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“…The antagonist EBN produces a small burst at the end of a saccade. This antagonistic rebound has been found experimentally (Van Gisbergen et al, 1981;Brown and Day, 1997), and may function as a braking pulse to decelerate the eye at the end of a saccade. Due to inhibition from one side of the SG on the other, as the activity of one TN increases, the activity of the other decreases by a similar amount.…”

Section: Methodsmentioning

confidence: 65%

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A neural model of the saccade generator in the reticular formation

Gancarz

Grossberg

1998

Neural Networks

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Section: Methodsmentioning

confidence: 65%

“…1). The model LLBNs show a prelude of activity, which is characteristic of the cell type (Van Gisbergen et al, 1981). The EBN burst begins after the onset of LLBN activity (Luschei and Fuchs, 1972).…”

Section: Methodsmentioning

confidence: 94%

A neural model of the saccade generator in the reticular formation

Gancarz

Grossberg

1998

Neural Networks

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“…In contrast, our patients with FTD-MND showed the vertical gaze abnormalities in early stages of the disease with a high frequency (72.7 %). Ocular motor neurons receive the final command for horizontal saccadic eye movements from burst neurons in the paramedian pontine reticular formation (PPRF) [35] and for vertical saccades from burst neurons in the riMLF, which lies in the prerubral fields of the rostral midbrain [8]. The total number of spikes in each burst of activity is proportional to the size of the eye movement.…”

Section: Discussionmentioning

confidence: 99%

“…The total number of spikes in each burst of activity is proportional to the size of the eye movement. That is, the saccadic eye movement is encoded by the temporal discharge of burst neurons [35]. Experimental or clinical lesions of the PPRF and riMLF abolish or slow saccades [7,11,12].…”

Section: Discussionmentioning

confidence: 99%

Slow vertical saccades in the frontotemporal dementia with motor neuron disease

et al. 2008

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“…20), which repre- sents where the eye should go (Robinson 1975;van Gisbergen et al 1981;Jürgens et al 1981;Scudder 1988;van Gisbergen and van Opstal 1989;Waitzman et al 1991). E d needs to be a sustained signal: it not only represents where to go but also drives the saccade.…”

Section: Spatial Aspects Of Saccadesmentioning

confidence: 99%

Reversible inactivation of macaque frontal eye field

1997

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The macaque frontal eye field (FEF) is involved in the generation of saccadic eye movements and fixations. To better understand the role of the FEF, we reversibly inactivated a portion of it while a monkey made saccades and fixations in response to visual stimuli. Lidocaine was infused into a FEF and neural inactivation was monitored with a nearby microelectrode. We used two saccadic tasks. In the delay task, a target was presented and then extinguished, but the monkey was not allowed to make a saccade to its location until a cue to move was given. In the step task, the monkey was allowed to look at a target as soon as it appeared. During FEF inactivation, monkeys were severely impaired at making saccades to locations of extinguished contralateral targets in the delay task. They were similarly impaired at making saccades to locations of contralateral targets in the step task if the target was flashed for ≤100 ms, such that it was gone before the saccade was initiated. Deficits included increases in saccadic latency, increases in saccadic error, and increases in the frequency of trials in which a saccade was not made. We varied the initial fixation location and found that the impairment specifically affected contraversive saccades rather than affecting all saccades made into head-centered contralateral space. Monkeys were impaired only slightly at making saccades to contralateral targets in the step task if the target duration was 1000 ms, such that the target was present during the saccade: latency increased, but increases in saccadic error were mild and increases in the frequency of trials in which a saccade was not made were insignificant. During FEF inactivation there usually was a direct correlation between the latency and the error of saccades made in response to contralateral targets. In the delay task, FEF inactivation increased the frequency of making premature saccades to ipsilateral targets. FEF inactivation had inconsistent and mild effects on saccadic peak velocity. FEF inactivation caused impairments in the ability to fixate lights steadily in contralateral space. FEF inactivation always caused an ipsiversive deviation of the eyes in darkness. In summary, our results suggest that the FEF plays major roles in (1) generating contraversive saccades to locations of extinguished or flashed targets, (2) maintaining contralateral fixations, and (3) suppressing inappropriate ipsiversive saccades.

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A quantitative analysis of generation of saccadic eye movements by burst neurons

Cited by 589 publications

References 14 publications

A neural model of the saccade generator in the reticular formation

A neural model of the saccade generator in the reticular formation

Slow vertical saccades in the frontotemporal dementia with motor neuron disease

Reversible inactivation of macaque frontal eye field

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