Premotor Inhibitory Neurons Carry Signals Related to Saccade Adaptation in the Monkey

2008 ◽  
Vol 99 (1) ◽  
pp. 220-230 ◽  
Author(s):  
Yoshiko Kojima ◽  
Yoshiki Iwamoto ◽  
Farrel R. Robinson ◽  
Christopher T. Noto ◽  
Kaoru Yoshida
Keyword(s):  
Gradual Increase ◽  
Cerebellar Nuclei ◽  
Inhibitory Neurons ◽  
Voluntary Movements ◽  
Burst Neurons ◽  
Premotor Neurons ◽  
Saccade Size ◽  
Motoneuron Activity ◽  
Saccade Adaptation ◽  
The Brain

Cerebellar output changes during motor learning. How these changes cause alterations of motoneuron activity and movement remains an unresolved question for voluntary movements. To answer this question, we examined premotor neurons for saccadic eye movement. Previous studies indicate that cells in the fastigial oculomotor region (FOR) within the cerebellar nuclei on one side exhibit a gradual increase in their saccade-related discharge as the amplitude of ipsiversive saccades adaptively decreases. This change in FOR activity could cause the adaptive change in saccade amplitude because neurons in the FOR project directly to the brain stem region containing premotor burst neurons (BNs). To test this possibility, we recorded the activity of saccade-related burst neurons in the area that houses premotor inhibitory burst neurons (IBNs) and examined their discharge during amplitude-reducing adaptation elicited by intrasaccadic target steps. We specifically analyzed their activity for off-direction (contraversive) saccades, in which the IBN activity would increase to reduce saccade size. Before adaptation, 29 of 42 BNs examined discharged, at least occasionally, for contraversive saccades. As the amplitude of contraversive saccades decreased adaptively, half of BNs with off-direction spike activity showed an increase in the number of spikes (14/29) or an earlier occurrence of spikes (7/14). BNs that were silent during off-direction saccades before adaptation remained silent after adaptation. These results indicate that the changes in the off-direction activity of BNs are closely related to adaptive changes in saccade size and are appropriate to cause these changes.

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.

Dynamic Coding of Vertical Facilitated Vergence by Premotor Saccadic Burst Neurons

2008 ◽  
Vol 100 (4) ◽  
pp. 1967-1982 ◽  
Author(s):  
Marion R. Van Horn ◽  
Kathleen E. Cullen
Keyword(s):  
Dimensional Space ◽  
Three Dimensional ◽  
Precise Control ◽  
Burst Neurons ◽  
Premotor Neurons ◽  
Horizontal Saccade ◽  
The Right ◽  
The Brain ◽  
Three Dimensional Space ◽  
Made In

To redirect our gaze in three-dimensional space we frequently combine saccades and vergence. These eye movements, known as disconjugate saccades, are characterized by eyes rotating by different amounts, with markedly different dynamics, and occur whenever gaze is shifted between near and far objects. How the brain ensures the precise control of binocular positioning remains controversial. It has been proposed that the traditionally assumed “conjugate” saccadic premotor pathway does not encode conjugate commands but rather encodes monocular commands for the right or left eye during saccades. Here, we directly test this proposal by recording from the premotor neurons of the horizontal saccade generator during a dissociation task that required a vergence but no horizontal conjugate saccadic command. Specifically, saccadic burst neurons (SBNs) in the paramedian pontine reticular formation were recorded while rhesus monkeys made vertical saccades made between near and far targets. During this task, we first show that peak vergence velocities were enhanced to saccade-like speeds (e.g., >150 vs. <100°/s during saccade-free movements for comparable changes in vergence angle). We then quantified the discharge dynamics of SBNs during these movements and found that the majority of the neurons preferentially encode the velocity of the ipsilateral eye. Notably, a given neuron typically encoded the movement of the same eye during horizontal saccades that were made in depth. Taken together, our findings demonstrate that the brain stem saccadic burst generator encodes integrated conjugate and vergence commands, thus providing strong evidence for the proposal that the classic saccadic premotor pathway controls gaze in three-dimensional space.

scholarly journals The Spatial and Cell-Type Distribution of SARS-CoV-2 Receptor ACE2 in the Human and Mouse Brains

2021 ◽  
Vol 11 ◽  
Author(s):  
Rongrong Chen ◽  
Keer Wang ◽  
Jie Yu ◽  
Derek Howard ◽  
Leon French ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Spatial Distribution ◽  
Host Cells ◽  
Inhibitory Neurons ◽  
Middle Temporal Gyrus ◽  
Distribution Analysis ◽  
Cell Type ◽  
Type Distribution ◽  
The Brain ◽  
Human And Mouse

By engaging angiotensin-converting enzyme 2 (ACE2 or Ace2), the novel pathogenic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) invades host cells and affects many organs, including the brain. However, the distribution of ACE2 in the brain is still obscure. Here, we investigated the ACE2 expression in the brain by analyzing data from publicly available brain transcriptome databases. According to our spatial distribution analysis, ACE2 was relatively highly expressed in some brain locations, such as the choroid plexus and paraventricular nuclei of the thalamus. According to cell-type distribution analysis, nuclear expression of ACE2 was found in many neurons (both excitatory and inhibitory neurons) and some non-neuron cells (mainly astrocytes, oligodendrocytes, and endothelial cells) in the human middle temporal gyrus and posterior cingulate cortex. A few ACE2-expressing nuclei were found in a hippocampal dataset, and none were detected in the prefrontal cortex. Except for the additional high expression of Ace2 in the olfactory bulb areas for spatial distribution as well as in the pericytes and endothelial cells for cell-type distribution, the distribution of Ace2 in the mouse brain was similar to that in the human brain. Thus, our results reveal an outline of ACE2/Ace2 distribution in the human and mouse brains, which indicates that the brain infection of SARS-CoV-2 may be capable of inducing central nervous system symptoms in coronavirus disease 2019 (COVID-19) patients. Potential species differences should be considered when using mouse models to study the neurological effects of SARS-CoV-2 infection.

scholarly journals Bilateral control of interceptive saccades: evidence from the ipsipulsion of vertical saccades after caudal fastigial inactivation

2021 ◽  
Author(s):  
Clara Bourrelly ◽  
Julie Quinet ◽  
Laurent Goffart
Keyword(s):  
Purkinje Cells ◽  
Visual Target ◽  
Strongly Correlated ◽  
Bilateral Control ◽  
Target Speed ◽  
Burst Neurons ◽  
Oculomotor Vermis ◽  
Vertical Saccades ◽  
Saccade Size ◽  
Saccade Velocity

The caudal fastigial nuclei (cFN) are the output nuclei by which the medio-posterior cerebellum influences the production of saccades toward a visual target. On the basis of the organization of their efferences to the premotor burst neurons and the bilateral control of saccades, the hypothesis was proposed that the same unbalanced activity accounts for the dysmetria of all saccades during cFN unilateral inactivation, regardless of whether the saccade is horizontal, oblique, or vertical. We further tested this hypothesis by studying, in two head-restrained macaques, the effects of unilaterally inactivating the caudal fastigial nucleus on saccades toward a target moving vertically with a constant, increasing or decreasing speed. After local muscimol injection, vertical saccades were deviated horizontally toward the injected side with a magnitude that increased with saccade size. The ipsipulsion indeed depended upon the tested target speed, but not its instantaneous value because it did not increase (decrease) when the target accelerated (decelerated). By subtracting the effect on contralesional horizontal saccades from the effect on ipsilesional ones, we found that the net bilateral effect on horizontal saccades was strongly correlated with the effect on vertical saccades. We explain how this correlation corroborates the bilateral hypothesis and provide arguments against the suggestion that instantaneous saccade velocity would somehow be "encoded" by the discharge of Purkinje cells in the oculomotor vermis.

Saccade Adaptation in Response to Altered Arm Dynamics

2003 ◽  
Vol 90 (6) ◽  
pp. 4016-4021 ◽  
Author(s):  
Thrishantha Nanayakkara ◽  
Reza Shadmehr
Keyword(s):  
Feedback Control ◽  
Real Time ◽  
Internal Model ◽  
Proprioceptive Feedback ◽  
Hand Position ◽  
Formidable Challenge ◽  
Random Direction ◽  
Intact Brain ◽  
Saccade Adaptation ◽  
The Brain

The delays in sensorimotor pathways pose a formidable challenge to the implementation of stable error feedback control, and yet the intact brain has little trouble maintaining limb stability. How is this achieved? One idea is that feedback control depends not only on delayed proprioceptive feedback but also on internal models of limb dynamics. In theory, an internal model allows the brain to predict limb position. Earlier we had found that during reaching, the brain estimates hand position in real-time in a coordinate system that can be used for generating saccades. Here we tested the idea that the estimate of hand position, as expressed through saccades, depends on an internal model that adapts to dynamics of the arm. We focused on the behavior of the eyes as perturbations were applied to the unseen hand. We found that when the hand was perturbed from stable posture with a 100-ms force pulse of random direction and magnitude, a saccade was generated on average at 182 ms postpulse onset to a position that was an unbiased estimate of real-time hand position. To test whether planning of saccades depended on an internal model of arm dynamics, arm dynamics were altered either predictably or unpredictably during the postpulse period. When arm dynamics were predictable, saccade amplitudes changed to reflect the change in the arm's behavior. We suggest that proprioceptive feedback from the arm is integrated into an adaptable internal model that computes an estimate of current hand position in eye-centered coordinates.

Fiber Microdissection Technique for Demonstrating the Deep Cerebellar Nuclei and Cerebellar Peduncles

2020 ◽  
Author(s):  
Nupur Pruthi ◽  
Paulo A S Kadri ◽  
Uğur Türe
Keyword(s):  
Cerebellar Nuclei ◽  
Operating Microscope ◽  
Deep Cerebellar Nuclei ◽  
Inferior Surface ◽  
Topographical Organization ◽  
Superior Surface ◽  
Cerebellar Peduncles ◽  
The Brain ◽  
Complex Parts ◽  
Formalin Fixed

Abstract BACKGROUND The cerebellum is one of the most primitive and complex parts of the human brain. The fiber microdissection technique can be extremely useful for neurosurgeons to understand the topographical organization of the cerebellum's important contents, such as the deep cerebellar nuclei and the cerebellar peduncles, and their relationship with the brain stem. OBJECTIVE To dissect the deep cerebellar nuclei and the cerebellar peduncles using the fiber microdissection technique. METHODS Under the operating microscope, 5 previously frozen, formalin-fixed human cerebellums and brain stems were dissected from the superior surface, and 5 were dissected from the inferior surface. Each stage of the process is described. The primary dissection tools were handmade, thin, wooden spatulas with tips of various sizes, toothpicks, and a fine regulated suction. RESULTS In 15 simplified dissection steps (6 for the superior surface and 9 for the inferior surface), the deep cerebellar nuclei (dentate, interpositus, and fastigial) and the cerebellar peduncles (inferior, middle, and superior) are delineated. Their anatomical relationships with each other and other neighboring structures are demonstrated. CONCLUSION The anatomy of the deep cerebellar nuclei and the cerebellar peduncles are clearly defined and understood through the use of the fiber microdissection technique. These stepwise dissections will guide the neurosurgeon in acquiring a topographical understanding of these complex and deep structures of the cerebellum. This knowledge, along with radiological information, can help in planning the most appropriate surgical strategy for various lesions of the cerebellum.

The coactivation of antagonist muscles

1981 ◽  
Vol 59 (7) ◽  
pp. 733-747 ◽  
Author(s):  
Allan M. Smith
Keyword(s):  
Purkinje Cells ◽  
Cerebellar Cortex ◽  
Precision Grip ◽  
Reciprocal Inhibition ◽  
Inhibitory Neurons ◽  
Voluntary Movements ◽  
Renshaw Cells ◽  
Power Grip ◽  
Antagonist Muscles ◽  
Antagonist Coactivation

Since Sherrington's convincing demonstration of the reciprocal innervation of opposing muscles, it has generally been thought that antagonist muscles are inactive during most voluntary movements. However, more recent evidence suggests that excitation of Renshaw cells may facilitate antagonist coactivation whereas excitation of Ia inhibitory neurons can induce reciprocal inhibition. A body of evidence has accumulated to indicate some of the circumstances which particularly favour the co-contraction of antagonist muscles. Isometric prehension, either in the precision grip or the power grip, can be shown to be one of the most important examples of antagonist coactivation. Studies of the discharge of single Purkinje cells of the intermediate cerebellar cortex in awake monkeys during performance of a maintained grip revealed that the majority of these neurons are deactivated during antagonist co-contraction. In contrast, other, unidentified neurons of the cerebellar cortex were as a group activated during grasping. It is suggested that the Purkinje cells act to inhibit antagonist muscles during reciprocal inhibition but are themselves inhibited during antagonist coactivation. These results support a suggestion made by Tilney and Pike in 1925 that the cerebellum plays an important role in switching between the coactivation and reciprocal inhibition of antagonist muscles.

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.

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.

MRI Findings in a Dog with Kernicterus

2013 ◽  
Vol 49 (4) ◽  
pp. 286-292 ◽  
Author(s):  
Katie M. Belz ◽  
Andrew J. Specht ◽  
Victoria S. Johnson ◽  
Julia A. Conway
Keyword(s):  
Total Bilirubin ◽  
Cerebellar Nuclei ◽  
Mri Findings ◽  
Caudate Nuclei ◽  
Neuronal Necrosis ◽  
Immune Mediated ◽  
Mixed Breed ◽  
Fluid Attenuated Inversion Recovery ◽  
Cortical Gray Matter ◽  
The Brain

A severe increase in total bilirubin coincided with a decline in neurologic status to comatose in a 9 yr old spayed female mixed-breed dog being treated for immune-mediated hemolytic anemia. MRI of the brain was performed to investigate potential causes for the neurologic signs. MRI revealed bilaterally symmetrical hyperintensities within the caudate nuclei, globus pallidus, thalamus, deep cerebellar nuclei, and cortical gray matter on T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences, which coincided with areas of bilirubin deposition and neuronal necrosis (kernicterus) identified on necropsy examination. This is the second case report of an adult dog exhibiting kernicterus, and the first report to document MRI findings associated with that condition. Kernicterus is an uncommonly reported complication of hyperbilirubinemia in dogs, but is potentially underreported due to difficulties in recognizing subtle lesions and distinguishing kernicterus from other potential causes of neurologic abnormalities with readily available antemortem tests. MRI may be helpful in supporting the diagnosis of kernicterus.

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