Fastigial Oculomotor Region and the Control of Foveation During Fixation

2010 ◽  
Vol 103 (4) ◽  
pp. 1988-2001 ◽  
Author(s):  
Lorenzo Guerrasio ◽  
Julie Quinet ◽  
Ulrich Büttner ◽  
Laurent Goffart
Keyword(s):  
Brain Stem ◽  
Visual Information ◽  
Visual Target ◽  
Target Position ◽  
Visual Fixation ◽  
Visually Guided ◽  
Cerebellar Lesions ◽  
Fixational Saccades ◽  
Fixation Offset ◽  
The Brain

When primates maintain their gaze directed toward a visual target (visual fixation), their eyes display a combination of miniature fast and slow movements. An involvement of the cerebellum in visual fixation is indicated by the severe gaze instabilities observed in patients suffering from cerebellar lesions. Recent studies in non-human primates have identified a cerebellar structure, the fastigial oculomotor region (FOR), as a major cerebellar output nucleus with projections toward oculomotor regions in the brain stem. Unilateral inactivation of the FOR leads to dysmetric visually guided saccades and to an offset in gaze direction when the animal fixates a visual target. However, the nature of this fixation offset is not fully understood. In the present work, we analyze the inactivation-induced effects on fixation. A novel technique is adopted to describe the generation of saccades when a target is being fixated (fixational saccades). We show that the offset is the result of a combination of impaired saccade accuracy and an altered encoding of the foveal target position. Because they are independent, we propose that these two impairments are mediated by the different projections of the FOR to the brain stem, in particular to the deep superior colliculus and the pontomedullary reticular formation. Our study demonstrates that the oculomotor cerebellum, through the activity in the FOR, regulates both the amplitude of fixational saccades and the position toward which the eyes must be directed, suggesting an involvement in the acquisition of visual information from the fovea.

Discharge Properties of Monkey Tectoreticular Neurons

2006 ◽  
Vol 95 (6) ◽  
pp. 3502-3511 ◽  
Author(s):  
C. Kip Rodgers ◽  
Douglas P. Munoz ◽  
Stephen H. Scott ◽  
Martin Paré
Keyword(s):  
Eye Movements ◽  
Brain Stem ◽  
Visual Information ◽  
Saccadic Eye Movements ◽  
Evoked Responses ◽  
Tonic Activity ◽  
Temporal Code ◽  
Intermediate Layers ◽  
Saccade Control ◽  
The Brain

The intermediate layers of the superior colliculus (SC) contain neurons that clearly play a major role in regulating the production of saccadic eye movements: a burst of activity from saccade neurons (SNs) is thought to provide a drive signal to set the eyes in motion, whereas the tonic activity of fixation neurons (FNs) is thought to suppress saccades during fixation. The exact contribution of these neurons to saccade control is, however, unclear because the nature of the signals sent by the SC to the brain stem saccade generation circuit has not been studied in detail. Here we tested the hypothesis that the SC output signal is sufficient to control saccades by examining whether antidromically identified tectoreticular neurons (TRNs: 33 SNs and 13 FNs) determine the end of saccades. First, TRNs had discharge properties similar to those of nonidentified SC neurons and a proportion of output SNs had visually evoked responses, which signify that the saccade generator must receive and process visual information. Second, only a minority of TRNs possessed the temporal patterns of activity sufficient to terminate saccades: Output SNs did not cease discharging at the time of saccade end, possibly continuing to drive the brain stem during postsaccadic fixations, and output FNs did not resume their activity before saccade end. These results argue against a role for SC in regulating the timing of saccade termination by a temporal code and suggest that other saccade centers act to thwart the extraneous SC drive signal, unless it controls saccade termination by a spatial code.

scholarly journals Abnormal tuning of saccade-related cells in pontine reticular formation of strabismic monkeys

2015 ◽  
Vol 114 (2) ◽  
pp. 857-868 ◽  
Author(s):  
Mark M. G. Walton ◽  
Michael J. Mustari
Keyword(s):  
Brain Stem ◽  
Reticular Formation ◽  
Binocular Vision ◽  
Visual Target ◽  
Saccadic Eye Movements ◽  
Abducens Nucleus ◽  
Vertical Saccades ◽  
Frequency Burst ◽  
The Brain ◽  
Oculomotor Abnormalities

Strabismus is a common disorder, characterized by a chronic misalignment of the eyes and numerous visual and oculomotor abnormalities. For example, saccades are often highly disconjugate. For humans with pattern strabismus, the horizontal and vertical disconjugacies vary with eye position. In monkeys, manipulations that disturb binocular vision during the first several weeks of life result in a chronic strabismus with characteristics that closely match those in human patients. Early onset strabismus is associated with altered binocular sensitivity of neurons in visual cortex. Here we test the hypothesis that brain stem circuits specific to saccadic eye movements are abnormal. We targeted the pontine paramedian reticular formation, a structure that directly projects to the ipsilateral abducens nucleus. In normal animals, neurons in this structure are characterized by a high-frequency burst of spikes associated with ipsiversive saccades. We recorded single-unit activity from 84 neurons from four monkeys (two normal, one exotrope, and one esotrope), while they made saccades to a visual target on a tangent screen. All 24 neurons recorded from the normal animals had preferred directions within 30° of pure horizontal. For the strabismic animals, the distribution of preferred directions was normal on one side of the brain, but highly variable on the other. In fact, 12/60 neurons recorded from the strabismic animals preferred vertical saccades. Many also had unusually weak or strong bursts. These data suggest that the loss of corresponding binocular vision during infancy impairs the development of normal tuning characteristics for saccade-related neurons in brain stem.

Equilibrium Disorder in Carbamazepine Toxicity

1977 ◽  
Vol 86 (3) ◽  
pp. 318-322 ◽  
Author(s):  
Yoshio Umeda ◽  
Eiji Sakata
Keyword(s):  
Brain Stem ◽  
Optokinetic Nystagmus ◽  
Speech Disorders ◽  
Clinical Findings ◽  
Cerebellar Lesions ◽  
Brain Stem Lesions ◽  
Stem Lesions ◽  
The Brain ◽  
Cerebellar Disorders ◽  
Space Occupying Lesion

Three cases of acute carbamazepine intoxication were evaluated neurotologically and neurologically. Findings included symptoms of equilibrium, gait and speech disorders, drowsiness, gaze nystagmus, depressed optokinetic nystagmus and disturbances of smooth pursuit eye movement. These findings, suggestive of a space-occupying lesion, disappeared after the cessation of the medication. On the basis of the clinical findings it is felt that carbamazepine affects structures within the brain stem and the cerebellum. It is well known that equilibrium disorders caused by anticonvulsant intoxication are due to cerebellar disorders but from our present study it should be noted that they originate not only from cerebellar lesions but also from brain stem lesions.

Three-Dimensional Eye Position and Slow Phase Velocity in Humans With Downbeat Nystagmus

2003 ◽  
Vol 89 (1) ◽  
pp. 338-354 ◽  
Author(s):  
S. Glasauer ◽  
M. Hoshi ◽  
U. Kempermann ◽  
T. Eggert ◽  
U. Büttner
Keyword(s):  
Brain Stem ◽  
Smooth Pursuit ◽  
Three Dimensional ◽  
Slow Phase ◽  
Downbeat Nystagmus ◽  
Gaze Holding ◽  
Fixation Task ◽  
Cerebellar Lesions ◽  
The Brain ◽  
Vestibular Pathways

Downbeat nystagmus (DN), a fixation nystagmus with the fast phases directed downward, is usually caused by cerebellar lesions, but the precise etiology is not known. A disorder of the smooth-pursuit system or of central vestibular pathways has been proposed. However, both hypotheses fail to explain why DN is usually accompanied by gaze-holding nystagmus, which implies a leaky neural velocity-to-position integrator. Because three-dimensional (3-D) analysis of nystagmus slow phases provides an excellent means for testing both hypotheses, we examined 19 patients with DN during a fixation task and compared them with healthy subjects. We show that the presentation of DN patients is not uniform; they can be grouped according to their deficits: DN with vertical integrator leakage, DN with vertical and horizontal integrator leakage, and DN without integrator leakage. The 3-D analysis of the slow phases of DN patients revealed that DN is most likely neither caused by damage to central vestibular pathways carrying semicircular canal information nor by a smooth pursuit imbalance. We propose that the observed effects can be explained by partial damage of a brain stem-cerebellar loop that augments the time constant of the neural velocity to position integrators in the brain stem and neurally adjusts the orientation of Listing's plane.

scholarly journals Act Quickly, Decide Later: Long-latency Visual Processing Underlies Perceptual Decisions but Not Reflexive Behavior

2011 ◽  
Vol 23 (12) ◽  
pp. 3734-3745 ◽  
Author(s):  
Jacob Jolij ◽  
H. Steven Scholte ◽  
Simon van Gaal ◽  
Timothy L. Hodgson ◽  
Victor A. F. Lamme
Keyword(s):  
Visual Processing ◽  
Visual Information ◽  
Task Demands ◽  
Conscious Awareness ◽  
Scene Segmentation ◽  
Visually Guided ◽  
Long Latency ◽  
Reflexive Behavior ◽  
Subjective Simultaneity ◽  
The Brain

Humans largely guide their behavior by their visual representation of the world. Recent studies have shown that visual information can trigger behavior within 150 msec, suggesting that visually guided responses to external events, in fact, precede conscious awareness of those events. However, is such a view correct? By using a texture discrimination task, we show that the brain relies on long-latency visual processing in order to guide perceptual decisions. Decreasing stimulus saliency leads to selective changes in long-latency visually evoked potential components reflecting scene segmentation. These latency changes are accompanied by almost equal changes in simple RTs and points of subjective simultaneity. Furthermore, we find a strong correlation between individual RTs and the latencies of scene segmentation related components in the visually evoked potentials, showing that the processes underlying these late brain potentials are critical in triggering a response. However, using the same texture stimuli in an antisaccade task, we found that reflexive, but erroneous, prosaccades, but not antisaccades, can be triggered by earlier visual processes. In other words: The brain can act quickly, but decides late. Differences between our study and earlier findings suggesting that action precedes conscious awareness can be explained by assuming that task demands determine whether a fast and unconscious, or a slower and conscious, representation is used to initiate a visually guided response.

Inhibition of Labyrinthine Nystagmus by Visual Fixation: Effects of Ablation of Visual Cortex and Superior Colliculi

1979 ◽  
Vol 88 (3) ◽  
pp. 419-423
Author(s):  
Emil P. Liebman ◽  
Joseph U. Toglia
Keyword(s):  
Visual Cortex ◽  
Visual System ◽  
Brain Stem ◽  
Light Stimulus ◽  
Visual Fixation ◽  
Vestibular Nystagmus ◽  
Superior Colliculi ◽  
Vestibular Testing ◽  
Significant Change ◽  
The Brain

A study was conducted to destroy two specific areas of the cat's visual system in order to determine if these lesions would affect the visual inhibition of calorically-induced vestibular nystagmus. The occipital visual cortex was removed in eight cats and the superior colliculi were removed bilaterally in nine cats. Postoperative vestibular testing revealed no significant change in the electronystagmography tracings and response to visual fixation. These findings suggest that, in cats, the visual inhibition of labyrinthine nystagmus is not dependent upon the integrity of the visual cortex or superior colliculi. The hypothesis is brought forward that the visual inhibition of the vestibular nystagmus is merely a reflex of the brain stem to light stimulus, mediated via the cerebellum.

Permeability of the microcirculation in area postrema of rat

1988 ◽  
Vol 46 ◽  
pp. 348-349
Author(s):  
Shams M. Ghoneim ◽  
Frank M. Faraci ◽  
Gary L. Baumbach
Keyword(s):  
Brain Stem ◽  
Area Postrema ◽  
Upper Body ◽  
Sprague Dawley ◽  
Sodium Cacodylate ◽  
Acute Hypertension ◽  
Sprague Dawley Rats ◽  
Ultrastructural Characteristics ◽  
The Brain ◽  
Adjacent Brain

The area postrema is a circumventricular organ in the brain stem and is one of the regions in the brain that lacks a fully functional blood-brain barrier. Recently, we found that disruption of the microcirculation during acute hypertension is greater in area postrema than in the adjacent brain stem. In contrast, hyperosmolar disruption of the microcirculation is greater in brain stem. The objective of this study was to compare ultrastructural characteristics of the microcirculation in area postrema and adjacent brain stem.We studied 5 Sprague-Dawley rats. Horseradish peroxidase was injected intravenously and allowed to circulate for 1, 5 or 15 minutes. Following perfusion of the upper body with 2.25% glutaraldehyde in 0.1 M sodium cacodylate, the brain stem was removed, embedded in agar, and chopped into 50-70 μm sections with a TC-Sorvall tissue chopper. Sections of brain stem were incubated for 1 hour in a solution of 3,3' diaminobenzidine tetrahydrochloride (0.05%) in 0.05M Tris buffer with 1% H2O2.

Surgical Approaches to the Brain Stem

1993 ◽  
Vol 4 (3) ◽  
pp. 457-468 ◽  
Author(s):  
Dennis Y. Wen ◽  
Roberto C. Heros
Keyword(s):  
Brain Stem ◽  
Surgical Approaches ◽  
The Brain

ADRENERGIC INPUTS TO THE AMYGDALA AND THE CONTROL OF GONADOTROPHIN RELEASE

1979 ◽  
Vol 90 (3) ◽  
pp. 385-393 ◽  
Author(s):  
José Borrell ◽  
Flavio Piva ◽  
Luciano Martini
Keyword(s):  
Brain Stem ◽  
Dopamine Receptor ◽  
Serum Levels ◽  
Female Rats ◽  
Receptor Blocker ◽  
Dopaminergic Drug ◽  
Gonadotrophin Secretion ◽  
Biphasic Effect ◽  
Adrenergic Blocker ◽  
The Brain

ABSTRACT Drugs able to mimic or to antagonize the action of catecholamines have been implanted bilaterally into the basomedial region of the amygdala of adult castrated female rats. The animals were killed at different intervals after the implantation of the different drugs, and serum levels of LH and FSH were measured by radioimmunoassay. The results have shown that the intra-amygdalar implantation of the alpha-adrenergic blocker phenoxybenzamine induces a significant increase of the release both of LH and FSH. The implantation of the beta-adrenergic blocker propranolol brings about a rise of LH only. The dopamine receptor blocker pimozide stimulates the release of LH and exerts a biphasic effect (stimulation followed by inhibition) of FSH secretion. The alpha-receptor stimulant clonidine and the dopaminergic drug 2-Br-alpha-ergocryptine were without significant effects. From these observations it is suggested that the adrenergic signals reaching the basomedial area of the amygdala (possibly from the brain stem) may be involved in the modulation of gonadotrophin secretion.

Sign in / Sign up

Export Citation Format

Share Document