scholarly journals Neural control of rapid binocular eye movements: Saccade-vergence burst neurons

2020 ◽  
Vol 117 (46) ◽  
pp. 29123-29132 ◽  
Author(s):  
Julie Quinet ◽  
Kevin Schultz ◽  
Paul J. May ◽  
Paul D. Gamlin
Keyword(s):  
Eye Movements ◽  
Neural Control ◽  
Three Dimensional ◽  
Mesencephalic Reticular Formation ◽  
Burst Neurons ◽  
Central Mesencephalic Reticular Formation ◽  
3D Space ◽  
Modeling Studies ◽  
Premotor Neurons ◽  
Highly Correlated

During normal viewing, we direct our eyes between objects in three-dimensional (3D) space many times a minute. To accurately fixate these objects, which are usually located in different directions and at different distances, we must generate eye movements with appropriate versional and vergence components. These combined saccade-vergence eye movements result in disjunctive saccades with a vergence component that is much faster than that generated during smooth, symmetric vergence eye movements. The neural control of disjunctive saccades is still poorly understood. Recent anatomical studies suggested that the central mesencephalic reticular formation (cMRF), located lateral to the oculomotor nucleus, contains premotor neurons potentially involved in the neural control of these eye movements. We have therefore investigated the role of the cMRF in the control of disjunctive saccades in trained rhesus monkeys. Here, we describe a unique population of cMRF neurons that, during disjunctive saccades, display a burst of spikes that are highly correlated with vergence velocity. Importantly, these neurons show no increase in activity for either conjugate saccades or symmetric vergence. These neurons are termed saccade-vergence burst neurons (SVBNs) to maintain consistency with modeling studies that proposed that such a class of neuron exists to generate the enhanced vergence velocities observed during disjunctive saccades. Our results demonstrate the existence and characteristics of SVBNs whose activity is correlated solely with the vergence component of disjunctive saccades and, based on modeling studies, are critically involved in the generation of the disjunctive saccades required to view objects in our 3D world.

Structure of the primate oculomotor burst generator. I. Medium-lead burst neurons with upward on-directions

1991 ◽  
Vol 65 (2) ◽  
pp. 203-217 ◽  
Author(s):  
A. K. Moschovakis ◽  
C. A. Scudder ◽  
S. M. Highstein
Keyword(s):  
Eye Movements ◽  
Mesencephalic Reticular Formation ◽  
Medial Longitudinal Fasciculus ◽  
Posterior Commissure ◽  
Inferior Rectus ◽  
Interstitial Nucleus Of Cajal ◽  
Burst Neurons ◽  
Physiological Characterization ◽  
Highly Correlated ◽  
Oculomotor Complex

1. To investigate the structure of the primate burst generator for vertical saccades, we obtained intra-axonal records from vertical medium-lead burst neurons with upward on-directions (UMLBs) in alert, behaving squirrel monkeys, while monitoring their spontaneous eye movements. After physiological characterization, these UMLBs were injected with horseradish peroxidase. 2. UMLBs (n = 14) had no spontaneous activity and emitted bursts of action potentials that preceded rapid eye movements by approximately 6 ms. Parameters of the burst (duration and number of spikes) were highly correlated with parameters of the rapid eye movement (duration and amplitude of the upward displacement of the eyes). 3. The axons of six UMLBs projected to the oculomotor complex. Their somata (4 were recovered) were all in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). Their axons traveled caudally in the medial longitudinal fasciculus (MLF) and ramified in the interstitial nucleus of Cajal (NIC) before entering the oculomotor nucleus. Five axons terminated bilaterally in the subdivisions innervating the superior rectus and inferior oblique muscles and therefore were presumed to be excitatory. One axon terminated in the ipsilateral inferior rectus and superior oblique subdivisions of the oculomotor complex and was presumed to be inhibitory. 4. Additionally, our data demonstrate that the nucleus of the posterior commissure (nPC) may also contain UMLBs. The axon of one such neuron crossed the midline within the posterior commissure and provided terminal fields to the contralateral nPC, riMLF, NIC, and the mesencephalic reticular formation but not to the oculomotor complex. 5. In conclusion, our data demonstrate that the rostral mesencephalon of the monkey contains neurons that have both the activity and the connections that are necessary either to provide motoneurons innervating extraocular muscles of both eyes with the pulse of activity they display during upward saccades or to inhibit their antagonists. Furthermore, our data demonstrate that some UMLBs are better suited for closing the feedback path of the local feedback loop rather than for providing direct input to extraocular motoneurons.

Saccadic Dyskinesia, Other Involuntary Eye Movements, and Gaze Deviations

2008 ◽  
Author(s):  
Agnes Wong
Keyword(s):  
Multiple Sclerosis ◽  
Eye Movements ◽  
Normal Subjects ◽  
Mesencephalic Reticular Formation ◽  
Frontal Eye Field ◽  
Square Wave ◽  
Central Mesencephalic Reticular Formation ◽  
Cerebellar Diseases ◽  
Eye Field ◽  
Small Saccade

■ A small saccade of 0.5–3° that takes the eye away from fixation, followed by a saccade that returns the eye back to fixation after about 200 msec (i.e., presence of intersaccadic interval during which visual feedback occurs) ■ So named because of its appearance in eye movement tracings ■ Normal subjects often have square wave jerks (SWJ), but the rate is only 4–6 per minute. ■ Pathologic SWJ occurs at a rate of >15 per minute. ■ Cerebellar diseases Square wave jerks result from damage of projections from the frontal eye field, rostral pole of the superior colliculus, and the central mesencephalic reticular formation to the omnipause cells in the pons. If symptomatic, SWJ may be treated with methylphenidate, diazepam, phenobarbital, or amphetamines. ■ Burst of saccades with defective steps of innervation (i.e., stepless saccades) ■ Conjugate or monocular Saccadic pulses are associated with multiple sclerosis. Saccadic pulses result from damage of omnipause cells or the neural integrator.

Response Properties of Saccade-Related Burst Neurons in the Central Mesencephalic Reticular Formation

1997 ◽  
Vol 78 (4) ◽  
pp. 2164-2175 ◽  
Author(s):  
Ari Handel ◽  
Paul W. Glimcher
Keyword(s):  
Reticular Formation ◽  
Light Emitting Diode ◽  
Low Frequency ◽  
Mesencephalic Reticular Formation ◽  
Restricted Range ◽  
Response Properties ◽  
Burst Neurons ◽  
Central Mesencephalic Reticular Formation ◽  
Saccadic Target ◽  
Behaving Monkeys

Handel, Ari and Paul W. Glimcher. Response properties of saccade-related burst neurons in the central mesencephalic reticular formation. J. Neurophysiol. 78: 2164–2175, 1997. We studied the activity of saccade-related burst neurons in the central mesencephalic reticular formation (cMRF) in awake behaving monkeys. In experiment 1, we examined the activity of single neurons while monkeys performed an average of 225 delayed saccade trials that evoked gaze shifts having horizontal and vertical amplitudes between 2 and 20°. All neurons studied generated high-frequency bursts of activity during some of these saccades. For each neuron, the duration and frequency of these bursts of activity reached maximal values when the monkey made movements within a restricted range of horizontal and vertical amplitudes. The onset of the movement followed the onset of the burst by the longest intervals for movements within a restricted range of horizontal and vertical amplitudes. The range of movements for which this interval was longest varied from neuron to neuron. Across the population, these ranges included nearly all contraversive saccades with horizontal and vertical amplitudes between 2 and 20°. In experiment 2, we used the following task to examine the low-frequency prelude of activity that cMRF neurons generate before bursting: the monkey was required to fixate a light-emitting diode (LED) while two eccentric visual stimuli were presented. After a delay, the color of the fixation LED was changed, identifying one of the two eccentric stimuli as the saccadic target. After a final unpredictable delay, the fixation LED was extinguished and the monkey was reinforced for redirecting gaze to the identified saccadic target. Some cMRF neurons fired at a low frequency during the interval after the fixation LED changed color but before it was extinguished. For many neurons, the firing rate during this interval was related to the metrics of the movement the monkey made at the end of the trial and, to a lesser degree, to the location of the eccentric stimulus to which a movement was not directed.

Central Positional Nystagmus Simulated by a Mathematical Ocular Motor Model of Otolith-Dependent Modification of Listing's Plane

2001 ◽  
Vol 86 (4) ◽  
pp. 1546-1554 ◽  
Author(s):  
S. Glasauer ◽  
M. Dieterich ◽  
Th. Brandt
Keyword(s):  
Eye Movements ◽  
Neural Control ◽  
Position Control ◽  
Three Dimensional ◽  
Head Tilt ◽  
Eye Position ◽  
Positional Nystagmus ◽  
Listing's Plane ◽  
Head Positions ◽  
Listing’S Plane

To find an explanation of the mechanisms of central positional nystagmus in neurological patients with posterior fossa lesions, we developed a three-dimensional (3-D) mathematical model to simulate head position-dependent changes in eye position control relative to gravity. This required a model implementation of saccadic burst generation, of the neural velocity to eye position integrator, which includes the experimentally demonstrated leakage in the torsional component, and of otolith-dependent neural control of Listing's plane. The validity of the model was first tested by simulating saccadic eye movements in different head positions. Then the model was used to simulate central positional nystagmus in off-vertical head positions. The model simulated lesions of assumed otolith inputs to the burst generator or the neural integrator, both of which resulted in different types of torsional-vertical nystagmus that only occurred during head tilt in roll plane. The model data qualitatively fit clinical observations of central positional nystagmus. Quantitative comparison with patient data were not possible, since no 3-D analyses of eye movements in various head positions have been reported in the literature on patients with positional nystagmus. The present model, prompted by an open clinical question, proposes a new hypothesis about the generation of pathological nystagmus and about neural control of Listing's plane.

Neural control of vergence eye movements: neurons encoding vergence velocity

1986 ◽  
Vol 56 (4) ◽  
pp. 1007-1021 ◽  
Author(s):  
L. E. Mays ◽  
J. D. Porter ◽  
P. D. Gamlin ◽  
C. A. Tello
Keyword(s):  
Eye Movements ◽  
Firing Rate ◽  
Neural Control ◽  
Mesencephalic Reticular Formation ◽  
State Behavior ◽  
Tonic Firing ◽  
Velocity Signal ◽  
Neural Organization ◽  
Vergence Movement ◽  
Disjunctive Eye Movements

Single-unit recordings were made from midbrain areas in monkeys trained to make both conjugate and disjunctive (vergence) eye movements. Previous work had identified cells with a firing rate proportional to the vergence angle, without regard to the direction of conjugate gaze. The present study describes the activity of neurons that burst for disjunctive eye movements. Convergence burst cells display a discrete burst of activity just before and during convergence eye movements. For most of these cells, the profile of the burst is correlated with instantaneous vergence velocity and the number of spikes in the burst is correlated with the size of the vergence movement. Some of these cells also have a tonic firing rate that is positively correlated with vergence angle (convergence burst-tonic cells). Divergence burst cells have similar properties, except that they fire for divergent and not convergent movements. Divergence burst cells are encountered far less often than convergence burst cells. Both convergence and divergence burst cells were found in an area of the mesencephalic reticular formation just dorsal and lateral to the oculomotor nucleus. Convergence burst cells were also recorded in another more dorsal mesencephalic region, rostral to the superior colliculus. Both of the areas also contain cells that encode vergence angle. Models of the vergence system derived from psychophysical data imply the existence of a vergence integrator, the output of which is vergence angle. Some models also suggest the presence of a parallel element that improves the frequency response of the vergence system, but has no effect on the steady-state behavior of the system. Vergence burst cells would be suitable inputs to a vergence integrator. By providing a vergence velocity signal to motoneurons, they may improve the dynamic response of the vergence system. The behavior of vergence burst cells during vergence movements is similar to that of the medium-lead burst cells during saccades. The proposed roles for vergence velocity cells are analogous to those of the saccadic burst cells. In this respect, the neural organization of the vergence system resembles that of the saccadic system, despite the distinct difference in the kinematics of these two types of eye movements.

scholarly journals Central mesencephalic reticular formation control of the near response: lens accommodation circuits

2019 ◽  
Vol 121 (5) ◽  
pp. 1692-1703 ◽  
Author(s):  
Paul J. May ◽  
Isabelle Billig ◽  
Paul D. Gamlin ◽  
Julie Quinet
Keyword(s):  
Rabies Virus ◽  
Reticular Formation ◽  
Formation Control ◽  
Present Report ◽  
Mesencephalic Reticular Formation ◽  
Time Frame ◽  
Medial Rectus ◽  
Depth Of Field ◽  
Central Mesencephalic Reticular Formation ◽  
Premotor Neurons

To view a nearby target, the three components of the near response are brought into play: 1) the eyes are converged through contraction of the medial rectus muscles to direct both foveae at the target, 2) the ciliary muscle contracts to allow the lens to thicken, increasing its refractive power to focus the near target on the retina, and 3) the pupil constricts to increase depth of field. In this study, we utilized retrograde transsynaptic transport of the N2c strain of rabies virus injected into the ciliary body of one eye of macaque monkeys to identify premotor neurons that control lens accommodation. We previously used this approach to label a premotor population located in the supraoculomotor area. In the present report, we describe a set of neurons located bilaterally in the central mesencephalic reticular formation that are labeled in the same time frame as the supraoculomotor area population, indicating their premotor character. The labeled premotor neurons are mostly multipolar cells, with long, very sparsely branched dendrites. They form a band that stretches across the core of the midbrain reticular formation. This population appears to be continuous with the premotor near-response neurons located in the supraoculomotor area at the level of the caudal central subdivision of the oculomotor nucleus. The central mesencephalic reticular formation has previously been associated with horizontal saccadic eye movements, so these premotor cells might be involved in controlling lens accommodation during disjunctive saccades. Alternatively, they may represent a population that controls vergence velocity. NEW & NOTEWORTHY This report uses transsynaptic transport of rabies virus to provide new evidence that the central mesencephalic reticular formation (cMRF) contains premotor neurons controlling lens accommodation. When combined with other recent reports that the cMRF also contains premotor neurons supplying medial rectus motoneurons, these results indicate that this portion of the reticular formation plays an important role in directing the near response and disjunctive saccades when viewers look between targets located at different distances.

Apparent Dissociation Between Saccadic Eye Movements and the Firing Patterns of Premotor Neurons and Motoneurons

1999 ◽  
Vol 82 (5) ◽  
pp. 2808-2811 ◽  
Author(s):  
Leo Ling ◽  
Albert F. Fuchs ◽  
James O. Phillips ◽  
Edward G. Freedman
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
High Frequency ◽  
Action Potentials ◽  
Saccadic Eye Movements ◽  
Line Of Sight ◽  
Movement Amplitude ◽  
Burst Neurons ◽  
Premotor Neurons ◽  
Motoneuron Activity

Saccadic eye movements result from high-frequency bursts of activity in ocular motoneurons. This phasic activity originates in premotor burst neurons. When the head is restrained, the number of action potentials in the bursts of burst neurons and motoneurons increases linearly with eye movement amplitude. However, when the head is unrestrained, the number of action potentials now increase as a function of the change in the direction of the line of sight during eye movements of relatively similar amplitudes. These data suggest an apparent uncoupling of premotor neuron and motoneuron activity from the resultant eye movement.

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