Vestibular and optokinetic nystagmus (OKN) of monkeys were induced by platform and visual surround rotation. Vision prolonged per-rotatory nystagmus and cancelled or reduced post-rotatory nystagmus recorded in darkness. Presumably, activity stored during OKN summed with activity arising in the semicircular canals. The limit of summation was about 120 degrees/s, the level of saturation of optokinetic after-nystagmus (OKAN). OKN and vestibular nystagmus, induced in the same or in opposite directions diminished or enhanced post-rotatory nystagmus up to 120 degrees/s. We postulate that a common storage mechanism is used for producing vestibular nystagmus, OKN, and OKAN. Evidence for this is the similar time course of vestibular nystagmus and OKAN and their summation. In addition, stored activity is lost in a similar way by viewing a stationary surround during either OKAN or vestibular nystagmus (fixation suppression). These responses were modelled using direct pathways and a non-ideal integrator coupled to the visual and peripheral vestibular systems. The direct pathways are responsible for rapid changes in eye velocity while the integrator stores activity and mediates slower changes. The integrator stabilizes eye velocity during whole field rotation and extends the time over which the vestibulo-ocular reflex can compensate for head movement.

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The central mesencephalic reticular formation (cMRF) was electrically stimulated in the alert monkey. Saccadic eye movements were induced to the contralateral side in the horizontal plane at latencies of 18-35 ms. Smooth or slow eye deviations were not produced by cMRF stimulation. If the stimulus was given during slow phases of nystagmus, rapid eye movements were elicited, and the velocity of the slow phases was not affected. The function of cMRF neurons and/or of pathways that lie within it appear primarily related to generation of rapid eye movements in the horizontal plane. The amplitude of induced saccadic eye movements depended solely on the region of cMRF that was activated. When the stimulation frequency was lower, the latency was longer, but the size and characteristics of the induced movement were the same. The product of latency and stimulus frequency was approximately constant, suggesting that saccades had been triggered after a fixed number of pulses had been given. Stimulation of cMRF at frequencies that were too low to elicit rapid eye movements had a tonic effect on saccade generation. When the animal was having optokinetic nystagmus (OKN), stimulation modulated beat frequency according to the direction of the nystagmus: contralateral quick phases were facilitated and ipsilateral quick phases were suppressed. The frequencies of stimulation necessary to suppress ipsilateral quick phases increased as slow phase eye velocity increased. This demonstrates that both cMRF activity and slow phase velocity affect quick phase triggering. When the cMRF on both sides were simultaneously stimulated, the eyes were fixed in place, and no further rapid movements occurred until the stimulus had ended. Thus, activity in pathways and/or cells in cMRF is not only able to trigger saccades, but can also change the excitability of saccade generating mechanisms and promote fixation by suppressing eye movements. Two types of rapid eye movements were elicited from cMRF. From dorsal portions of cMRF saccades were induced whose size was relatively constant and not dependent on the initial position of the eyes in the orbit. The size of saccades increased from small to large as the stimulating electrode was advanced through cMRF from dorsal to ventral. This suggests that the tecto-bulbo-spinal efferents coursing through cMRF and/or cMRF neurons related to this input, are organized in a topographic fashion, with cells and fibers related to eye movements of increasing size being layered one beneath another.(ABSTRACT TRUNCATED AT 400 WORDS)