Connections of behaviorally identified cat omnipause neurons

1978 ◽  
Vol 32 (3) ◽  
Author(s):  
W.M. King ◽  
W. Precht ◽  
N. Dieringer
Keyword(s):  
Omnipause Neurons

Saccade–Vergence Interactions in Macaques. I. Test of the Omnipause Multiply Model

2005 ◽  
Vol 94 (4) ◽  
pp. 2295-2311 ◽  
Author(s):  
C. Busettini ◽  
L. E. Mays
Keyword(s):  
Eye Movements ◽  
Main Sequence ◽  
Peak Velocity ◽  
Alternative Models ◽  
Omnipause Neurons ◽  
Velocity Enhancement

Horizontal vergence eye movements are movements in opposite directions used to change fixation between far and near targets. The occurrence of a saccade during vergence causes vergence velocity to be transiently enhanced. The goal of this study was to test in the monkey the previously described Multiply Model (Zee et al. 1992) that holds that, in humans, the speeding of vergence during a saccade may be the result of the disinhibition of a subgroup of vergence-related neurons by the saccadic omnipause neurons (OPNs). In agreement with the Multiply Model: 1) the onset of the enhancement was closely related to saccadic onset, and thus linked to the onset of the OPN pause; 2) the magnitude of the vergence velocity enhancement was strongly dependent on saccade–vergence timing. Contrary to the Multiply Model: 1) the peak of the vergence velocity enhancement was dependent on saccadic peak velocity; 2) the dependency on saccadic peak velocity was not the indirect result of a dependency on saccadic duration and therefore on the duration of the OPN pause; 3) the decline of the vergence enhancement, identified by the time of the peak of the enhancement velocity, occurred too early to be linked to the end of the OPN pause; 4) vergence enhancement had a saccadic-like peak-velocity/size main sequence. Overall, the evidence is incompatible with the OPN Multiply hypothesis of vergence enhancement. Alternative models are described in an accompanying paper.

Activity of monkey frontal eye field neurons projecting to oculomotor regions of the pons

1992 ◽  
Vol 68 (6) ◽  
pp. 1967-1985 ◽  
Author(s):  
M. A. Segraves
Keyword(s):  
Electrical Stimulation ◽  
Visual Stimulation ◽  
Saccadic Eye Movements ◽  
Frontal Eye Field ◽  
Related Activity ◽  
Burst Neurons ◽  
Eye Field ◽  
Movement Field ◽  
Omnipause Neurons ◽  
Stimulation Of

1. This study identified neurons in the rhesus monkey's frontal eye field that projected to oculomotor regions of the pons and characterized the signals sent by these neurons from frontal eye field to pons. 2. In two behaving rhesus monkeys, frontal eye field neurons projecting to the pons were identified via antidromic excitation by a stimulating microelectrode whose tip was centered in or near the omnipause region of the pontine raphe. This stimulation site corresponded to the nucleus raphe interpositus (RIP). In addition, electrical stimulation of the frontal eye field was used to demonstrate the effects of frontal eye field input on neurons in the omnipause region and surrounding paramedian pontine reticular formation (PPRF). 3. Twenty-five corticopontine neurons were identified and characterized. Most frontal eye field neurons projecting to the pons were either movement neurons, firing in association with saccadic eye movements (48%), or foveal neurons responsive to visual stimulation of the fovea combined with activity related to fixation (28%). Corticopontine movement neurons fired before, during, and after saccades made within a restricted movement field. 4. The activity of identified corticopontine neurons was very similar to the activity of neurons antidromically excited from the superior colliculus where 59% had movement related activity, and 22% had foveal and fixation related activity. 5. High-intensity, short-duration electrical stimulation of the frontal eye field caused omnipause neurons to stop firing. The cessation in firing appeared to be immediate, within < or = 5 ms. The time that the omnipause neuron remained quiet depended on the intensity of the cortical stimulus and lasted up to 30 ms after a train of three stimulus pulses lasting a total of 6 ms at an intensity of 1,000 microA. Low-intensity, longer duration electrical stimuli (24 pulses, 75 microA, 70 ms) traditionally used to evoke saccades from the frontal eye field were also followed by a cessation in omnipause neuron firing, but only after a delay of approximately 30 ms. For these stimuli, the omnipause neuron resumed firing when the stimulus was turned off. 6. The same stimuli that caused omnipause neurons to stop firing excited burst neurons in the PPRF. The latency to excitation ranged from 4.2 to 9.8 ms, suggesting that there is at least one additional neuron between frontal eye field neurons and burst neurons in the PPRF. 7. The present study confirms and extends the results of previous work, with the use of retrograde and anterograde tracers, demonstrating direct projections from the frontal eye field to the pons.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Saccade-Related Inhibitory Input to Pontine Omnipause Neurons: An Intracellular Study in Alert Cats

1999 ◽  
Vol 82 (3) ◽  
pp. 1198-1208 ◽  
Author(s):  
Kaoru Yoshida ◽  
Yoshiki Iwamoto ◽  
Sohei Chimoto ◽  
Hiroshi Shimazu
Keyword(s):  
Initial Phase ◽  
Time Course ◽  
Inhibitory Input ◽  
Peak Time ◽  
Time Integral ◽  
Intracellular Study ◽  
Afferent Discharge ◽  
Alert Cats ◽  
Eye Velocity ◽  
Omnipause Neurons

Omnipause neurons (OPNs) are midline pontine neurons that are thought to control a number of oculomotor behaviors, especially saccades. Intracellular recordings were made from OPNs in alert cats to elucidate saccade-associated postsynaptic events in OPNs and thereby determine what patterns of afferent discharge impinge on OPNs to cause their saccadic inhibition. The membrane potential of impaled OPNs exhibited steep hyperpolarization before each saccade that lasted for the whole period of the saccade. The hyperpolarization was reversed to depolarization by intracellular injection of Cl− ions, indicating it consisted of temporal summation of inhibitory postsynaptic potentials (IPSPs). The duration of the saccade-related hyperpolarization was almost equal to the duration of the concurrent saccades. The time course of the hyperpolarization was similar to that of the radial eye velocity except for the initial phase. During the falling phase of eye velocity, the correlation between the instantaneous amplitude of hyperpolarization and the instantaneous eye velocity was highly significant. The amplitude of hyperpolarization at the eye velocity peak was correlated significantly with the peak eye velocity. The time integral of the hyperpolarization was correlated with the radial amplitude of saccades. The initial phase disparity between the hyperpolarization and eye velocity was due to the relative constancy of peak time (∼20 ms) of the initial steep hyperpolarization regardless of the later potential profile that covaried with the eye velocity. The initial steep hyperpolarization led the beginning of saccades by 15.9 ± 3.8 (SD) ms, which is longer than the lead time for medium-lead burst neurons. These results demonstrate that the pause of activity in OPNs is caused by IPSPs initiated by an abrupt, intense input and maintained, for the whole duration of the saccade, by afferents conveying eye velocity signals. We suggest that the initial sudden inhibition originates from central structures such as the superior colliculus and frontal eye fields and that the eye velocity-related inhibition originates from the burst generator in the brain stem.

Common Inhibitory Mechanism for Saccades and Smooth-Pursuit Eye Movements

2002 ◽  
Vol 88 (4) ◽  
pp. 1880-1892 ◽  
Author(s):  
M. Missal ◽  
E. L. Keller
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Statistical Significance ◽  
Smooth Pursuit Eye Movements ◽  
Inhibitory Mechanism ◽  
Inhibitory System ◽  
Electrical Microstimulation ◽  
Pursuit Eye Movements ◽  
Premotor Neurons ◽  
Omnipause Neurons

The premotor pathways subserving saccades and smooth-pursuit eye movements are usually thought to be different. Indeed, saccade and smooth-pursuit eye movements have different dynamics and functions. In particular, a group of midline cells in the pons called omnipause neurons (OPNs) are considered to be part of the saccadic system only. It has been established that OPNs keep premotor neurons for saccades under constant inhibition during fixation periods. Saccades occur only when the activity of OPNs has completely stopped or paused. Accordingly, electrical stimulation in the region of OPNs inhibits premotor neurons and interrupts saccades. The premotor relay for smooth pursuit is thought to be organized differently and omnipause neurons are not supposed to be involved in smooth-pursuit eye movements. To investigate this supposition, OPNs were recorded during saccades and during smooth pursuit in the monkey ( Macaca mulatta). Unexpectedly, we found that neuronal activity of OPNs decreased during smooth pursuit. The resulting activity reduction reached statistical significance in ∼50% of OPNs recorded during pursuit of a target moving at 40°/s. On average, activity was reduced by 34% but never completely stopped or paused. The onset of activity reduction coincided with the onset of smooth pursuit. The duration of activity reduction was correlated with pursuit duration and its intensity was correlated with eye velocity. Activity reduction was observed even in the absence of catch-up saccades that frequently occur during pursuit. Electrical microstimulation in the OPNs' area induced a strong deceleration of the eye during smooth pursuit. These results suggest that OPNs form an inhibitory mechanism that could control the time course of smooth pursuit. This inhibitory mechanism is part of the fixation system and is probably needed to avoid reflexive eye movements toward targets that are not purposefully selected. This study shows that saccades and smooth pursuit, although they are different kinds of eye movements, are controlled by the same inhibitory system.

Brain Stem Omnipause Neurons and the Control of CombinedEye-Head Gaze Saccades in the Alert Cat

1998 ◽  
Vol 79 (6) ◽  
pp. 3060-3076 ◽  
Author(s):  
Martin Paré ◽  
Daniel Guitton
Keyword(s):  
Gaze Control ◽  
Error Signal ◽  
Gaze Shifts ◽  
Gaze Shift ◽  
The Gaze ◽  
Alert Cat ◽  
Motor Error ◽  
Omnipause Neurons ◽  
Gaze Saccades ◽  
Stimulation Of

Paré, Martin and Daniel Guitton. Brain stem omnipause neurons and the control of combined eye-head gaze saccades in the alert cat. J. Neurophysiol. 79: 3060–3076, 1998. When the head is unrestrained, rapid displacements of the visual axis—gaze shifts (eye-re-space)—are made by coordinated movements of the eyes (eye-re-head) and head (head-re-space). To address the problem of the neural control of gaze shifts, we studied and contrasted the discharges of omnipause neurons (OPNs) during a variety of combined eye-head gaze shifts and head-fixed eye saccades executed by alert cats. OPNs discharged tonically during intersaccadic intervals and at a reduced level during slow perisaccadic gaze movements sometimes accompanying saccades. Their activity ceased for the duration of the saccadic gaze shifts the animal executed, either by head-fixed eye saccades alone or by combined eye-head movements. This was true for all types of gaze shifts studied: active movements to visual targets; passive movements induced by whole-body rotation or by head rotation about stationary body; and electrically evoked movements by stimulation of the caudal part of the superior colliculus (SC), a central structure for gaze control. For combined eye-head gaze shifts, the OPN pause was therefore not correlated to the eye-in-head trajectory. For instance, in active gaze movements, the end of the pause was better correlated with the gaze end than with either the eye saccade end or the time of eye counterrotation. The hypothesis that cat OPNs participate in controlling gaze shifts is supported by these results, and also by the observation that the movements of both the eyes and the head were transiently interrupted by stimulation of OPNs during gaze shifts. However, we found that the OPN pause could be dissociated from the gaze-motor-error signal producing the gaze shift. First, OPNs resumed discharging when perturbation of head motion briefly interrupted a gaze shift before its intended amplitude was attained. Second, stimulation of caudal SC sites in head-free cat elicited large head-free gaze shifts consistent with the creation of a large gaze-motor-error signal. However, stimulation of the same sites in head-fixed cat produced small “goal-directed” eye saccades, and OPNs paused only for the duration of the latter; neither a pause nor an eye movement occurred when the same stimulation was applied with the eyes at the goal location. We conclude that OPNs can be controlled by neither a simple eye control system nor an absolute gaze control system. Our data cannot be accounted for by existing models describing the control of combined eye-head gaze shifts and therefore put new constraints on future models, which will have to incorporate all the various signals that act synergistically to control gaze shifts.

Activity of omnipause neurons in alert cats during saccadic eye movements and visual stimuli

1982 ◽  
Vol 47 (5) ◽  
pp. 827-844 ◽  
Author(s):  
C. Evinger ◽  
C. R. Kaneko ◽  
A. F. Fuchs
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Visual Stimuli ◽  
Pause Duration ◽  
Visual Input ◽  
Transient Increase ◽  
Abducens Nucleus ◽  
Wide Range ◽  
Area Centralis ◽  
Omnipause Neurons

1. In the cats trained to follow a target spot with their eyes, activity was recorded from omnipause neurons (OPNs). OPNs discharge at a relatively high steady tonic rate (50-130 spikes/s) during visual fixation and smooth-pursuit eye movements but exhibit a complete cessation of discharge that begins before saccades in any direction. They are located in a compact region of the dorsal pontine tegmentum near the midline, just rostral to the abducens nucleus. 2. The average duration of the horizontal or vertical component of a saccade increases monotonically with pause duration, but a given pause duration is associated with a large range of individual saccade parameters and the timing of the pause, such as the latency from the pause onset to saccade onset or the interval from the maximum saccade velocity to the end of the pause, is no better. However, OPNs can be divided into two distinct groups on the basis of the timing of the pause relative to the parameters of the saccade. One group ceases discharging 32.4 +/- 4.6 ms, on average, before the saccade, while the second pauses 18.2 +/- 3.4 ms before the saccade. 3. Microstimulation at the site of OPNs affects the occurrence and trajectory of saccades but not smooth pursuit or fixation. Sustained electrical stimulation (20 micro A) lasting several seconds prevents the occurrence of saccades while brief trains (10-60 ms), timed to occur early in the saccade, interrupt it in midflight for the duration of the train. The latency to the interruption is about 26 ms. These data support the view that OPNs tonically inhibit the saccadic machinery between saccades and must be turned off to allow a saccade to occur. 4. Almost every (65 of 69) feline OPN exhibited a brief transient increase in activity for visual stimuli moving in any direction with a wide range of velocities. A moving 1 degree spot was generally more effective than a moving full-field, striped background. All units also showed a transient increase in firing when the spot was turned either on or off. Receptive fields plotted with the spot were greater than 250 deg2 and always included the area centralis. Two-thirds of the cells tested also responded to auditory stimuli. 5. Interaction between the excitatory visual input and the saccade-related pause was tested by comparing OPN activity and the saccadic trajectory during eye movements in the dark versus the light and by presenting brief flashes of light during a saccade. During saccades in the dark, the steady firing of OPNs was less than during saccades in the light. Only by stabilizing a flashed spot of light to occur on the area centralis at the beginning of the saccade was it possible to activate an OPN artificially to interrupt the saccade in midflight. Therefore, rather than being instrumental in specifically controlling the saccade trajectory, the visual input, along with the auditory and other sensory inputs, probably serves, under normal visual conditions, to help establish the tonic rate of OPNs. 6...

A new local feedback model of the saccadic burst generator

1988 ◽  
Vol 59 (5) ◽  
pp. 1455-1475 ◽  
Author(s):  
C. A. Scudder
Keyword(s):  
Target Position ◽  
Burst Frequency ◽  
Experimental Conditions ◽  
Burst Neurons ◽  
Feedback Model ◽  
Long Duration ◽  
Important Input ◽  
Local Feedback ◽  
The Brain ◽  
Omnipause Neurons

1. To accommodate the finding that the superior colliculus is an important input to the brain stem pathways that generate saccades (the saccadic burst generator), a new model of the burst generator is proposed. Unlike the model of Robinson (61) from which it was derived, the model attempts to match a neural replica of change in eye position, which is the output of the burst generator, to a neural replica of change in target position, which is the output of the colliculus and the input to the model. 2. The elements of the model correspond to neurons known or thought to be associated with the actual primate saccadic burst generator and are mostly connected together in accord with the results of anatomical and physiological experiments. 3. The model was simulated on a digital computer to compare its behavior with that of the actual burst generator under normal and experimental conditions. Simulated peak burst frequency and saccade duration matched that obtained from monkey excitatory burst neurons and inhibitory burst neurons for saccades up to 15 degrees but did not match at larger sizes; stimulation of the omnipause neurons caused an interruption of the saccade, and the saccade resumed at the end of stimulation as in actual data; the model can generate the abnormally long-duration saccades seen under decreased alertness or various pathologies by changing the burst generator inputs and without having to change any properties of the neurons themselves or their connections; a simulated horizontal and vertical burst generator pair connected only through the omnipause neurons can generate realistic oblique saccades. 4. The implications of the model for higher-order control of the saccadic burst generator are discussed.

scholarly journals The behavioural and neurophysiological modulation of microsaccades in monkeys

2009 ◽  
Vol 3 (2) ◽  
Author(s):  
Donald C. Brien ◽  
Brian D. Corneil ◽  
Jillian H. Fecteau ◽  
Andrew H. Bell ◽  
Douglas P. Munoz
Keyword(s):  
Visual Cues ◽  
Human Studies ◽  
Separate Experiment ◽  
Suitable Model ◽  
Auditory Cues ◽  
Covert Orienting ◽  
Omnipause Neurons

Systematic modulations of microsaccades have been observed in humans during covert orienting. We show here that monkeys are a suitable model for studying the neurophysiology governing these modulations of microsaccades. Using various cue-target saccade tasks, we observed the effects of visual and auditory cues on microsaccades in monkeys. As in human studies, following visual cues there was an early bias in cue-congruent microsaccades followed by a later bias in cue-incongruent microsaccades. Following auditory cues there was a cue-incongruent bias in left cues only. In a separate experiment, we observed that brainstem omnipause neurons, which gate all saccades, also paused during microsaccade generation. Thus, we provide evidence that at least part of the same neurocircuitry governs both large saccades and microsaccades.

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