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.

Structure of the primate oculomotor burst generator. II. Medium-lead burst neurons with downward on-directions

1991 ◽  
Vol 65 (2) ◽  
pp. 218-229 ◽  
Author(s):  
A. K. Moschovakis ◽  
C. A. Scudder ◽  
S. M. Highstein ◽  
J. D. Warren
Keyword(s):  
Mesencephalic Reticular Formation ◽  
Medial Longitudinal Fasciculus ◽  
Inferior Rectus ◽  
Interstitial Nucleus Of Cajal ◽  
Burst Neurons ◽  
Downward Displacement ◽  
Highly Correlated ◽  
Discharge Patterns ◽  
Superior Oblique ◽  
Oculomotor Complex

1. To investigate the morphology and physiology of vertical medium-lead burst neurons with downward on-directions (DMLBs), we impaled midbrain axons and recorded their discharge patterns in relation to spontaneous saccades of alert, behaving squirrel monkeys. Selected axons were injected with horseradish peroxidase and morphologically characterized. 2. DMLBs emitted bursts of impulses that preceded rapid eye movements by approximately 5 ms. Parameters of the burst (duration and number of spikes) were highly correlated with parameters of the saccadic eye movement (duration and amplitude of the downward displacement of the eyes). 3. Somata of DMLBs were recovered in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF, n = 14), and in the interstitial nucleus of Cajal (NIC, n = 2). Fibers originating from riMLF DMLBs projected, usually ipsilaterally, to the NIC as well as in the inferior rectus and the superior oblique subdivisions of the oculomotor complex. The axons of NIC DMLBs projected to the ipsilateral riMLF, NIC, and the mesencephalic reticular formation but not to the oculomotor complex. 4. Our data demonstrate that some DMLBs can provide extraocular motoneurons of both eyes with the pulse of activity they display during downward saccades. In addition, such neurons can supply the NIC with one of the signals that this nucleus is thought to integrate to extract an estimate of the vertical eye position. Finally, our data demonstrate the existence of DMLBs that do not establish direct connections with oculomotoneurons.

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.

Anatomy and physiology of the primate interstitial nucleus of Cajal I. efferent projections

1996 ◽  
Vol 75 (2) ◽  
pp. 725-739 ◽  
Author(s):  
T. Kokkoroyannis ◽  
C. A. Scudder ◽  
C. D. Balaban ◽  
S. M. Highstein ◽  
A. K. Moschovakis
Keyword(s):  
Superior Colliculus ◽  
Reticular Formation ◽  
Mesencephalic Reticular Formation ◽  
Head Movements ◽  
Zona Incerta ◽  
Medial Longitudinal Fasciculus ◽  
Thalamic Nuclei ◽  
Posterior Commissure ◽  
Interstitial Nucleus Of Cajal ◽  
Efferent Projections

1. The efferent projections of the interstitial nucleus of Cajal (NIC) were studied in the squirrel monkey after iontophoretic injections of biocytin and Phaseolus Vulgaris leucoagglutinin into the NIC. To ensure the proper placement of the tracer, the same pipettes were used to extracellularly record the discharge pattern of NIC neurons. 2. Three projection systems of the NIC were distinguished: commissural (through the posterior commissure), descending, and ascending. 3. The posterior commissure system gave rise to dense terminal fields in the contralateral NIC, the oculomotor nucleus, and the trochlear nucleus. 4. The descending system of NIC projections deployed dense terminal fields in the ipsilateral gigantocellular reticular formation and the paramedian reticular formation of the pons, as well as in the ventromedial and commissural nuclei of the first two spinal cervical segments. It also gave rise to moderate or weak terminal fields in the vestibular complex, the nucleus prepositus hypoglossi, the inferior olive, and the magnocellular reticular formation, as well as cell groups scattered along the paramedian tracts in the pons and the pontine and medullary raphe. 5. The ascending system of NIC projections gave rise to dense terminal fields in the ipsilateral mesencephalic reticular formation and the zona incerta as well as moderate or weak terminal fields in the ipsilateral centromedian and parafascicular thalamic nuclei. It also provided dense bilateral labeling of the rostral interstitial nucleus of the medial longitudinal fasciculus and the fields of Forel, and moderate or weak bilateral labeling of the mediodorsal, central medial, and central lateral nuclei of the thalamus. 6. Models of saccade generation that rely on feedback from the velocity-to-position integrators and include the superior colliculus in their local feedback loop are contradicted because no fibers originating from the NIC traveled to the superior colliculus to deploy terminal fields. 7. Consistent with its morphological and functional diversity, these data indicate that the primate NIC sends signals to a multitude of targets implicated in the control of eye and head movements.

Activity of Mesencephalic Vertical Burst Neurons During Saccades and Smooth Pursuit

2000 ◽  
Vol 83 (4) ◽  
pp. 2080-2092 ◽  
Author(s):  
M. Missal ◽  
S. de Brouwer ◽  
P. Lefèvre ◽  
E. Olivier
Keyword(s):  
Vertical Velocity ◽  
Smooth Pursuit ◽  
Medial Longitudinal Fasciculus ◽  
Eye Position ◽  
Interstitial Nucleus Of Cajal ◽  
Burst Neurons ◽  
Preferred Direction ◽  
Saccade Onset ◽  
Vertical Saccades ◽  
Eye Velocity

The activity of vertical burst neurons (BNs) was recorded in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF-BNs) and in the interstitial nucleus of Cajal (NIC-BNs) in head-restrained cats while performing saccades or smooth pursuit. BNs emitted a high-frequency burst of action potentials before and during vertical saccades. On average, these bursts led saccade onset by 14 ± 4 ms (mean ± SD, n = 23), and this value was in the range of latencies (∼5–15 ms) of medium-lead burst neurons (MLBNs). All NIC-BNs ( n = 15) had a downward preferred direction, whereas riMLF-BNs showed either a downward ( n = 3) or an upward ( n = 5) preferred direction. We found significant correlations between saccade and burst parameters in all BNs: vertical amplitude was correlated with the number of spikes, maximum vertical velocity with maximum of the spike density, and saccade duration with burst duration. A correlation was also found between instantaneous vertical velocity and neuronal activity during saccades. During fixation, all riMLF-BNs and ∼50% of NIC-BNs (7/15) were silent. Among NIC-BNs active during fixation (8/15), only two cells had an activity correlated with the eye position in the orbit. During smooth pursuit, most riMLF-BNs were silent (7/8), but all NIC-BNs showed an activity that was significantly correlated with the eye velocity. This activity was unaltered during temporary disappearance of the visual target, demonstrating that it was not visual in origin. For a given neuron, its on-direction during smooth pursuit and saccades remained identical. The activity of NIC-BNs during both saccades and smooth pursuit can be described by a nonlinear exponential function using the velocity of the eye as independent variable. We suggest that riMLF-BNs, which were not active during smooth pursuit, are vertical MLBNs responsible for the generation of vertical saccades. Because NIC-BNs discharged during both saccades and pursuit, they cannot be regarded as MLBNs as usually defined. NIC-BNs could, however, be the site of convergence of both the saccadic and smooth pursuit signals at the premotoneuronal level. Alternatively, NIC-BNs could participate in the integration of eye velocity to eye position signals and represent input neurons to a common integrator.

Vertical eye movement-related secondary vestibular neurons ascending in medial longitudinal fasciculus in cat. II. Direct connections with extraocular motoneurons

1990 ◽  
Vol 63 (4) ◽  
pp. 918-935 ◽  
Author(s):  
Y. Iwamoto ◽  
T. Kitama ◽  
K. Yoshida
Keyword(s):  
Rectus Muscle ◽  
Medial Longitudinal Fasciculus ◽  
Field Potentials ◽  
Oculomotor Nucleus ◽  
Inferior Rectus ◽  
Interstitial Nucleus Of Cajal ◽  
Excitatory Connection ◽  
Superior Rectus ◽  
Spike Triggered Averaging ◽  
Trochlear Nucleus

1. The preceding study in the alert cat has shown that many secondary vestibular axons that ascend in the medial longitudinal fasciculus (MLF) increase their firing rate in proportion to downward eye position. In the present study, projection and termination of these downward-position-vestibular (DPV) neurons within extraocular motoneuron pools were studied electrophysiologically by spike-triggered averaging techniques and morphologically be reconstructing their axonal trajectory after intra-axonal injection of horseradish peroxidase (HRP). 2. Extracellular field potentials recorded within the trochlear nucleus and/or the inferior rectus subdivision of the oculomotor nucleus were averaged by the use of spike potentials of single DPV neurons as triggers. All the crossed-DPV axons tested induced negative unitary field potentials in the trochlear nucleus (n = 9) and in the inferior rectus subdivision of the oculomotor nucleus (n = 5), suggesting that they made monosynaptic excitatory connection with motoneurons in these nuclei. The four crossed-DPV axons tested in the two motoneuron pools induced unitary field potentials in both. The majority of crossed-DPV axons terminated in these nuclei were directly activated from the caudal MLF, indicating that they had descending collaterals projecting to the spinal cord as well. The uncrossed-DPV axons did not induce such unitary field potentials either in the trochlear nucleus (n = 4) or in the inferior rectus subdivision (n = 3). 3. All the uncrossed-DPV axons examined (n = 14) induced positive unitary field potentials in the superior rectus subdivision of the oculomotor nucleus, suggesting that they made monosynaptic inhibitory connections with motoneurons innervating the superior rectus muscle. These uncrossed-DPV axons displayed regular firing patterns and were not activated from the caudal MLF. None of the crossed-DPV axons tested (n = 4) induced unitary field potentials in the superior rectus subdivision. 4. Five crossed-DPV axons were injected with HRP. All these axons ascended in the MLF contralateral to their soma, gave off many collaterals to the trochlear nucleus, and projected more rostrally. For three well-stained axons, numerous terminal branches were also found in the rostroventral part of the contralateral oculomotor nucleus, the area corresponding to the inferior rectus subdivision. Some collaterals in the oculomotor nucleus recrossed the midline to terminate in the medial part of the ipsilateral oculomotor nucleus. Other terminations were observed in the interstitial nucleus of Cajal and in the periaqueductal gray adjacent to the oculomotor nucleus. The crossed axons injected included both regular and irregular types, and three of the four examined were activated from the caudal MLF.(ABSTRACT TRUNCATED AT 400 WORDS)

Disorders of Ocular Motility Due to Disease of the Brainstem, Cerebellum, and Diencephalon

2015 ◽  
pp. 836-915
Author(s):  
R. John Leigh ◽  
David S. Zee
Keyword(s):  
Developmental Disorders ◽  
Medial Longitudinal Fasciculus ◽  
Ocular Motility ◽  
Posterior Commissure ◽  
Interstitial Nucleus Of Cajal ◽  
Abducens Nucleus ◽  
Cerebellar Syndromes ◽  
Vertical Gaze ◽  
Dorsal Midbrain Syndrome ◽  
Gaze Palsy

This chapter reviews clinical features (with illustrative video cases) and pathophysiology of medullary lesions, including Wallenberg’s syndrome and oculopalatal tremor. Manifestations and pathophysiology of three cerebellar syndromes are described (flocculus and paraflocculus, nodulus and ventral uvula, dorsal vermis and fastigial nucleus), applying these principles to interpret the effects of developmental disorders (e.g., Chiari malformation), hereditary ataxia, paraneoplastic cerebellar degeneration, cerebellar stroke, and cerebellar tumors. Characteristics of pontine lesions are discussed, including lesions of the abducens nucleus, paramedian pontine reticular formation (PPRF), internuclear ophthalmoplegia (INO), one-and-a-half syndrome, slow horizontal saccades, and saccadic oscillations. The effects of midbrain lesions are summarized, including lesions affecting the rostral interstitial nucleus of the medial longitudinal fasciculus (RIMLF), interstitial nucleus of Cajal, posterior commissure, and more diffuse processes causing slow vertical saccades or vertical gaze palsy (dorsal midbrain syndrome), including Whipple’s disease. Effects of lesions affecting the superior colliculus, thalamus, and pulvinar are also discussed.

Loss of Ipsidirectional Quick Phases of Torsional Nystagmus with a Unilateral Midbrain Lesion1

1993 ◽  
Vol 3 (2) ◽  
pp. 115-121
Author(s):  
R. John Leigh ◽  
Scott H. Seidman ◽  
Michael P. Grant ◽  
Joseph P. Hanna
Keyword(s):  
Eye Movements ◽  
Medial Longitudinal Fasciculus ◽  
Unilateral Lesion ◽  
Interstitial Nucleus Of Cajal ◽  
Torsional Nystagmus

We report a patient with a long-standing, unilateral lesion of the midbrain who showed ipsidirectional loss of torsional quick phases, impairment of all vertical eye movements and normal horizontal eye movements. The findings are consistent with recent reports of the effects of experimental lesions, in monkeys, of the,rostral interstitial nucleus of the medial longitudinal fasciculus and the interstitial nucleus of Cajal.

The Neural Basis for Conjugate Eye Movements

2015 ◽  
pp. 386-473
Author(s):  
R. John Leigh ◽  
David S. Zee
Keyword(s):  
Posterior Parietal Cortex ◽  
Visual Area ◽  
Medial Longitudinal Fasciculus ◽  
Descending Pathways ◽  
Adaptive Optimization ◽  
Focal Lesions ◽  
Posterior Commissure ◽  
Interstitial Nucleus Of Cajal ◽  
Medial Superior Temporal ◽  
Dorsolateral Prefrontal

This chapter draws on a range of studies of macaque and humans to forge an anatomical scheme for the control of gaze. At each stage, this scheme is used to predict effects of focal lesions on the control of gaze, with video examples. Contributions include the abducens nucleus, medial longitudinal fasciculus (MLF), and paramedian pontine reticular formation (PPRF) to horizontal gaze; the rostral interstitial nucleus of the medial longitudinal fasciculus (RIMLF), interstitial nucleus of Cajal, and posterior commissure to vertical gaze; cerebellar flocculus, paraflocculus, dorsal vermis, fastigial nucleus, and inferior olive to adaptive optimization of gaze. Cortical control of gaze by structures including primary visual cortex (V1), middle temporal visual area (MT, V5), medial superior temporal visual area (MST), posterior parietal cortex, frontal eye fields, supplementary eye fields, dorsolateral prefrontal cortex, cingulate cortex, descending pathways, thalamus, pulvinar, caudate, substantia nigra pars reticulata, subthalamic nucleus, and superior colliculus are each discussed.

Effects of Reversible Inactivation of the Primate Mesencephalic Reticular Formation. II. Hypometric Vertical Saccades

2000 ◽  
Vol 83 (4) ◽  
pp. 2285-2299 ◽  
Author(s):  
David M. Waitzman ◽  
Valentine L. Silakov ◽  
Stacy DePalma-Bowles ◽  
Amanda S. Ayers
Keyword(s):  
Reticular Formation ◽  
Main Sequence ◽  
Mesencephalic Reticular Formation ◽  
Medial Longitudinal Fasciculus ◽  
Saccade Amplitude ◽  
Burst Neurons ◽  
Vertical Saccades ◽  
Vertical Saccade ◽  
Omnipause Neurons ◽  
Saccade Duration

Electrical microstimulation and single-unit recording have suggested that a group of long-lead burst neurons (LLBNs) in the mesencephalic reticular formation (MRF) just lateral to the interstitial nucleus of Cajal (INC) (the peri-INC MRF, piMRF) may play a role in the generation of vertical rapid eye movements. Inactivation of this region with muscimol (a GABAA agonist) rapidly produced vertical saccade hypometria (6 injections). In three of six injections, there was a marked reduction in the velocity of vertical saccades out of proportion to saccade amplitude (i.e., saccades fell below the main sequence). This was associated with a moderate increase in saccade duration. Inadvertent inactivation of the INC could not account for these observations because vertical, postsaccadic drift was not observed. Similarly, pure downward saccade hypometria, the hallmark of rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) inactivation, was always preceded by loss of upward saccades in our experiments. We also found a downward and ipsiversive displacement of initial eye position and evidence of a contraversive head tilt following piMRF injections. Saccade latency was shorter after two of six injections. Simulation of a local feedback model provided three possible explanations for vertical saccade hypometria: 1) a shift in the input to the model to request smaller saccades, 2) a reduction of LLBN input to the vertical saccade medium lead burst neurons (MLBNs), or 3) an increase in the gain of the feedback pathway. However, when the second hypothesis was coupled to a shortened duration of the saccade trigger (i.e., the discharge of the omnipause neurons), the physiological observations of piMRF inactivation could be replicated. This suggested that muscimol had targeted structures that provided both long-lead burst activity to the MLBNs in the riMLF and were critical for reactivation of the omnipause neurons. Evidence of markedly reduced vertical saccade amplitude, curved saccade trajectories, increased saccade duration, and saccades that fall below the amplitude/velocity main sequence in these monkeys closely parallels the oculomotor findings of patients with progressive supranuclear palsy (PSP).

scholarly journals Understanding Parinaud’s Syndrome

2021 ◽  
Vol 11 (11) ◽  
pp. 1469
Author(s):  
Juan Fernando Ortiz ◽  
Ahmed Eissa-Garces ◽  
Samir Ruxmohan ◽  
Victor Cuenca ◽  
Mandeep Kaur ◽  
...  
Keyword(s):  
Visual Field ◽  
Light Stimulus ◽  
Medial Longitudinal Fasciculus ◽  
Visual Field Defects ◽  
Superior Cerebellar Peduncle ◽  
Eyelid Retraction ◽  
Posterior Commissure ◽  
Interstitial Nucleus Of Cajal ◽  
Parinaud’S Syndrome ◽  
Field Defects

Parinaud’s syndrome involves dysfunction of the structures of the dorsal midbrain. We investigated the pathophysiology related to the signs and symptoms to better understand the symptoms of Parinaud’s syndrome: diplopia, blurred vision, visual field defects, ptosis, squint, and ataxia, and Parinaud’s main signs of upward gaze paralysis, upper eyelid retraction, convergence retraction nystagmus (CRN), and pseudo-Argyll Robertson pupils. In upward gaze palsy, three structures are disrupted: the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), interstitial nucleus of Cajal (iNC), and the posterior commissure. In CRN, there is a continuous discharge of the medial rectus muscle because of the lack of inhibition of supranuclear fibers. In Collier’s sign, the posterior commissure and the iNC are mainly involved. In the vicinity of the iNC, there are two essential groups of cells, the M-group cells and central caudal nuclear (CCN) group cells, which are important for vertical gaze, and eyelid control. Overstimulation of the M group of cells and increased firing rate of the CCN group causing eyelid retraction. External compression of the posterior commissure, and pretectal area causes pseudo-Argyll Robertson pupils. Pseudo-Argyll Robertson pupils constrict to accommodation and have a slight response to light (miosis) as opposed to Argyll Robertson pupils were there is no response to a light stimulus. In Parinaud’s syndrome patients conserve a slight response to light because an additional pathway to a pupillary light response that involves attention to a conscious bright/dark stimulus. Diplopia is mainly due to involvement of the trochlear nerve (IVth cranial nerve. Blurry vision is related to accommodation problems, while the visual field defects are a consequence of chronic papilledema that causes optic neuropathy. Ptosis in Parinaud’s syndrome is caused by damage to the oculomotor nerve, mainly the levator palpebrae portion. We did not find a reasonable explanation for squint. Finally, ataxia is caused by compression of the superior cerebellar peduncle.

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