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The saccade trigger signal was proposed by D.A. Robinson, but neural substrates for triggering saccades by inhibiting omnipause neuron (OPN) activity still remain controversial. We investigated tectal inputs to OPNs by recording intracellular potentials from OPNs and inhibitory burst neurons (IBNs) and searched for interneurons to inhibit OPNs in the brainstem of anesthetized cats. IBNs received monosynaptic excitation from the contralateral caudal superior colliculus (SC) and disynaptic inhibition via contralateral IBNs from the ipsilateral caudal SC, whereas IBNs received disynaptic inhibition from the rostral SC. The latter disynaptic inhibition was mediated by OPNs, since OPNs received monosynaptic excitation from the rostral SC and projected to IBNs. In contrast, OPNs received disynaptic inhibition from the caudal SC. This disynaptic inhibition from the caudal SC was mediated to OPNs by IBNs. These findings suggested possible roles of IBNs for triggering and maintaining saccades by actively inhibiting the tonic activity of OPNs., (© 2011 New York Academy of Sciences.)

The caudal part of the superior colliculus (SC) plays an important role in the generation of saccades, whereas the rostral part of the SC is considered to be involved in visual fixation. The present study was performed to determine neural connections from the rostral and caudal parts of the SC to inhibitory burst neurons (IBNs) and pause neurons (PNs) in the nucleus raphe interpositus in the anesthetized cat, and to reveal the functional role of the rostral SC on eye movements. The intracellular potentials from IBNs and PNs were recorded, and the effects of stimulation of the SC on these neurons were analyzed. The results show that IBNs receive monosynaptic excitation from the contralateral caudal SC, and disynaptic inhibition from the ipsilateral caudal SC via contralateral IBNs. In addition, IBNs receive disynaptic inhibition from the rostral part of the SC on either side via inhibitory interneurons other than IBNs. Intracellular recording from PNs revealed that they receive convergent excitation from the rostral parts of the bilateral superior colliculi and that the rostral SC inhibits IBNs on both sides via PNs. The neural connections determined in this study support the functional independence of the rostral SC and are consistent with the notion that the "fixation zone" is localized in the rostral SC. These results show that the fixation zone in the rostral SC may suppress the initiation of bilateral saccades via pause neurons.

After a saccadic eye movement occurs to an interesting object appearing in the visual field, visual fixation holds its image on the fovea and suppresses saccades to other objects appearing in the visual field. To understand the neural mechanism of visual fixation, the effects of electrical stimulation of the frontal eye field (FEF) on the generation of electrically evoked saccades (Esacs) and the suppression of saccades in trained monkeys were investigated. When the properties of the electrically evoked suppression of visually guided (Vsacs) and memory-guided saccades (Msacs) were examined, two types of suppression were found. Stimulation of a wide area of the FEF suppressed only ipsiversive Vsacs and Msacs at stimulus intensities lower than those for eliciting Esacs, whereas stimulation of a localized area of the FEF suppressed the initiation of both Vsacs and Msacs in any direction during and approximately 50 ms after stimulation. However, neither stimulation affected the vector of these saccades. The thresholds for suppression were usually less than 50 microA. The most effective stimulation timing for the suppression of ipsiversive and contraversive Vsacs was approximately 40 to 50 ms before saccade onset. Therefore, suppression occurred in the efferent pathway for Vsacs at the premotor rather than the motoneuronal level, most likely in the superior colliculus and/or the paramedian pontine reticular formation. The results suggest that the suppression in the FEF may play a role in maintaining visual fixation by suppressing the generation of saccades.

Vestibular input to the periarcuate cortex in the Japanese monkey was examined by analyzing laminar field potentials evoked by electrical stimulation of the vestibular nerve. Vestibular-evoked potentials consisted of early-positive and late-negative potentials and early-negative and late-positive potentials in the superficial and deep layers of the cortex, respectively. They were distributed bilaterally in the periarcuate cortex around the junction of the spur and the arcuate sulcus. This vestibular-projecting area corresponded to the periarcuate area where retrogradely-labeled corticovestibular neurons were distributed after the injection of a tracer into the vestibular nuclei. Comparison of the vestibular-projection area with the distribution of smooth pursuit-related neurons in the same monkey revealed that such neurons existed in the vestibular-projecting area of the periarcuate cortex.