Neural control of saccadic eye movements

Sparks, David L.; Barton, Ellen J.

doi:10.1016/0959-4388(93)90169-y

Cited by 41 publications

(25 citation statements)

References 26 publications

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“…These discharge properties and the changes in the acceleration of ipsilesional saccades reported in the present study are compatible with the hypothesis of a "bilateral" (rather than "push-pull") mechanism by which the activity from saccade related neurons in both cFN regulates the balance between the inhibitory and excitatory input to the ocular motoneurons pool (see Fig. 10 in Goffart et al 2004; see also Goffart 2007;Sparks and Barton 1993). In this hypothesis, the increase in eye peak velocity would be due to the removal by cFN inactivation of an inhibition that contralateral inhibitory burst neurons (off-direction burst) exert on motoneurons innervating the agonist muscles.…”

Section: Comparison With Studies In the Head-restrained Monkeysupporting

confidence: 78%

Head-Unrestrained Gaze Shifts After Muscimol Injection in the Caudal Fastigial Nucleus of the Monkey

Quinet¹,

Goffart²

2007

Journal of Neurophysiology

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The effects of unilateral cFN inactivation on horizontal and vertical gaze shifts generated from a central target toward peripheral ones were tested in two head unrestrained monkeys. After muscimol injection, the eye component was hypermetric during ipsilesional gaze shifts, hypometric during contralesional ones and deviated toward the injected side during vertical gaze shifts. The ipsilesional gaze hypermetria increased with target eccentricity until ϳ24°after which it diminished and became smaller than the hypermetria of the eye component. Contrary to eye saccades, the amplitude and peak velocity of which were enhanced, the amplitude and peak velocity of head movements were reduced during ipsilesional gaze shifts. These changes in head movement were not correlated with those affecting the eye saccades. Head movements were also delayed relative to the onset of eye saccades. The alterations in head movement and the faster eye saccades likely explained the reduced head contribution to the amplitude of ipsilesional gaze shifts. The contralesional gaze hypometria increased with target eccentricity and was associated with uncorrelated reductions in eye and head peak velocities. When compared with control movements of similar amplitude, contralesional eye saccades had lower peak velocity and longer duration. This slowing likely accounted for the increase in head contribution to the amplitude of contralesional gaze shifts. These data suggest different pathways for the fastigial control of eye and head components during gaze shifts. Saccade dysmetria was not compensated by appropriate changes in head contribution, raising the issue of the feedback control of movement accuracy during combined eyehead gaze shifts.

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Section: Comparison With Studies In the Head-restrained Monkeysupporting

confidence: 78%

Head-Unrestrained Gaze Shifts After Muscimol Injection in the Caudal Fastigial Nucleus of the Monkey

Quinet¹,

Goffart²

2007

Journal of Neurophysiology

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“…In the following text, we propose an alternative view for understanding all the deficits that are induced by cFN inactivation. This view emphasizes the bilateral organization of cFN influence on the brain stem control of saccades (Sparks and Barton 1993). The period when the saccade-related neurons in both left and right cFN are simultaneously bursting is very important for understanding the dysmetria of saccades during cFN inactivation, whether the saccade is horizontal, oblique, or vertical.…”

Section: Deficits In Saccadementioning

confidence: 99%

Deficits in Saccades and Fixation During Muscimol Inactivation of the Caudal Fastigial Nucleus in the Rhesus Monkey

Goffart

Chen²,

Sparks³

2004

Journal of Neurophysiology

111

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The caudal fastigial nucleus (cFN) is a major nucleus by which the cerebellum influences the accuracy of saccades. In head-restrained monkeys generating saccades from a fixation light-emitting diode (LED) toward a flashed target LED, we analyzed the effects of unilateral pharmacological inactivation of cFN on horizontal, vertical, and oblique saccades. When animals were viewing the fixation LED, usually after one or more correction saccades, the positions of the eyes were slightly offset in comparison with the positions maintained before the injection (average offset = 1.1 degrees). The offset was ipsilateral to the injected side and did not depend on the target location. The horizontal component of all ipsilesional saccades was hypermetric and associated with a 32-42% increase in the amplitude of the deceleration displacement without significant change in the amplitude of the acceleration displacement. The horizontal component of all contralesional saccades was hypometric and associated with a decrease in the peak velocity and in the acceleration amplitude (30-35% decrease) without significant change in the deceleration amplitude. The amplitude of vertical saccades was not systematically affected, but their trajectory was always deviated toward the injected side. They missed the target with an error that depended on saccade duration or amplitude. If any, the effects of muscimol injections on the vertical component of oblique saccades were very small. The changes in fixation and the dysmetria are both viewed as consequences of an impairment in the cFN bilateral influence on the burst neurons located in the left and right brain stem.

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“…Moreover, according to Sparks (1991), the eyes and head of subjects move in the same direction only until the eyes reach their oculomotor limit or until the line of sight is directed at the target. Than, usually, the head continues to move and the eyes move in the opposite direction, compensating for the still ongoing head movement.…”

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confidence: 99%