scholarly journals Adaptive control of movement deceleration during saccades

2021 ◽  
Vol 17 (7) ◽  
pp. e1009176
Author(s):  
Simon P. Orozco ◽  
Scott T. Albert ◽  
Reza Shadmehr
Keyword(s):  
Current Model ◽  
Error Sensitivity ◽  
Subsequent Trial ◽  
Adaptive Processes ◽  
Acceleration Period ◽  
Acceleration And Deceleration ◽  
Visual Error ◽  
Two State Model ◽  
The Brain ◽  
A Current

As you read this text, your eyes make saccades that guide your fovea from one word to the next. Accuracy of these movements require the brain to monitor and learn from visual errors. A current model suggests that learning is supported by two different adaptive processes, one fast (high error sensitivity, low retention), and the other slow (low error sensitivity, high retention). Here, we searched for signatures of these hypothesized processes and found that following experience of a visual error, there was an adaptive change in the motor commands of the subsequent saccade. Surprisingly, this adaptation was not uniformly expressed throughout the movement. Rather, after experience of a single error, the adaptive response in the subsequent trial was limited to the deceleration period. After repeated exposure to the same error, the acceleration period commands also adapted, and exhibited resistance to forgetting during set-breaks. In contrast, the deceleration period commands adapted more rapidly, but suffered from poor retention during these same breaks. State-space models suggested that acceleration and deceleration periods were supported by a shared adaptive state which re-aimed the saccade, as well as two separate processes which resembled a two-state model: one that learned slowly and contributed primarily via acceleration period commands, and another that learned rapidly but contributed primarily via deceleration period commands.

scholarly journals Spontaneous recovery and the multiple timescales of human motor memory

2020 ◽  
Author(s):  
Simon P. Orozco ◽  
Scott T. Albert ◽  
Reza Shadmehr
Keyword(s):  
Spontaneous Recovery ◽  
Temporal Dynamics ◽  
Current Model ◽  
The Other ◽  
Independent Learning ◽  
Motor Memory ◽  
Adaptive Controllers ◽  
Error Sensitivity ◽  
Adaptive Processes ◽  
Acceleration Period

AbstractIn numerous paradigms, from fear conditioning to motor adaptation, memory exhibits a remarkable property: acquisition of a novel behavior followed by its extinction results in spontaneous recovery of the original behavior. A current model suggests that spontaneous recovery occurs because learning is supported by two different adaptive processes: one fast (high error sensitivity, low retention), and the other slow (low error sensitivity, high retention). Here, we searched for signatures of these hypothesized processes in the commands that guided single movements. We examined human saccadic eye movements and observed that following experience of a visual error, there was an adaptive change in the motor commands of the subsequent saccade, partially correcting for the error. However, the error correcting commands were expressed only during the deceleration period. If the errors persisted, the acceleration period commands also changed. Adaptation of acceleration period commands exhibited poor sensitivity to error, but the learning was resistant to forgetting. In contrast, the deceleration period commands adapted with high sensitivity to error, and the learning suffered from poor retention. Thus, within a single saccade, a fast-like process influenced the deceleration period commands, whereas a slow-like process influenced the acceleration period commands. Following extinction training, with passage of time motor memory exhibited spontaneous recovery, as evidenced by return of saccade endpoints toward their initial adapted state. The temporal dynamics of spontaneous recovery suggested that a single saccade is controlled by two different adaptive controllers, one active during acceleration, and the other during deceleration.Significance statementA feature of memory in many paradigms is the phenomenon of spontaneous recovery: learning followed by extinction inevitably leads to reversion toward the originally learned behavior. A theoretical model posits that spontaneous recovery is a feature of memory systems that learn with two independent learning processes, one fast, and the other slow. However, there have been no direct measures of these putative processes. Here, we found potential signatures of the two independent adaptive processes during control of a single saccade. The results suggest that distinct adaptive controllers contribute to the acceleration and deceleration phases of a saccade, and that each controller is supported by a fast and a slow learning process.

scholarly journals Sensitivity to prediction error in reach adaptation

2012 ◽  
Vol 108 (6) ◽  
pp. 1752-1763 ◽  
Author(s):  
Mollie K. Marko ◽  
Adrian M. Haith ◽  
Michelle D. Harran ◽  
Reza Shadmehr
Keyword(s):  
Prediction Error ◽  
Sensory Feedback ◽  
Error Signal ◽  
Single Trial ◽  
Subsequent Trial ◽  
Error Magnitude ◽  
Sensory Modalities ◽  
Visual Error ◽  
The Brain ◽  
Complex Spikes

It has been proposed that the brain predicts the sensory consequences of a movement and compares it to the actual sensory feedback. When the two differ, an error signal is formed, driving adaptation. How does an error in one trial alter performance in the subsequent trial? Here we show that the sensitivity to error is not constant but declines as a function of error magnitude. That is, one learns relatively less from large errors compared with small errors. We performed an experiment in which humans made reaching movements and randomly experienced an error in both their visual and proprioceptive feedback. Proprioceptive errors were created with force fields, and visual errors were formed by perturbing the cursor trajectory to create a visual error that was smaller, the same size, or larger than the proprioceptive error. We measured single-trial adaptation and calculated sensitivity to error, i.e., the ratio of the trial-to-trial change in motor commands to error size. We found that for both sensory modalities sensitivity decreased with increasing error size. A reanalysis of a number of previously published psychophysical results also exhibited this feature. Finally, we asked how the brain might encode sensitivity to error. We reanalyzed previously published probabilities of cerebellar complex spikes (CSs) and found that this probability declined with increasing error size. From this we posit that a CS may be representative of the sensitivity to error, and not error itself, a hypothesis that may explain conflicting reports about CSs and their relationship to error.

Abstract TP147: Central Post Stroke Pain: A Systematic Review

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jonathan Singer ◽  
Alyssa Conigliaro ◽  
Elizabeth Spina ◽  
Susan Law ◽  
Steven Levine
Keyword(s):  
Systematic Review ◽  
Brain Imaging ◽  
Pain Scale ◽  
Post Stroke ◽  
Underlying Causes ◽  
Single Question ◽  
Thalamic Region ◽  
The Brain ◽  
A Current

Background: Central Post Stroke Pain (CPSP) is reportedly due to strokes in the thalamic region (Dishinbition Theory); however, the Central Imbalance Theory states that CPSP is due to damage to the spinothalamic pathway (STP). Aims: 1) Clarify the role of thalamic strokes and STP damage in CPSP patients. 2) Gain a current understanding of anatomic substrates, brain imaging, and treatment of CPSP. Methods: Two independent reviewers systematically reviewed PUBMED, CINAHL and Web of Science for studies including original, clinical studies and randomized controlled trials (RCTs) using PRISMA guidelines. Studies had to assess CPSP, using a single question or pain scale. Results: Search from January – July 2016, identifying 731 publications. We extracted data from 23 studies and categorized the articles’ aims into 4 sections: somatosensory deficits (5 studies), STP (3 studies), brain imaging (7 studies), and RCTs (8 studies). Somatosensory studies showed high rates of CPSP; however, the underlying causes of these deficits were unclear. Most studies did not refer to stroke location as playing a role in CPSP, but that pathways may. STP studies displayed consistent evidence that the STP plays a major role in CPSP, delineating that CPSP can occur even when the stroke is not in the thalamic region but in other regions (e.g. cerebellum, basal ganglia, medulla). Four of the brain imaging studies found CPSP not related and 3 found it was related to thalamic strokes. All 7 studies had major limitations including sample size, no control groups, and selection bias. RCTs were mostly negative, but brain stem and motor cortex stimulation studies showed the most promise. Conclusions: While CPSP has been linked to the thalamic region since the early 1900’s, the peer-reviewed literature showed equivocal results when examining location of stroke. Our systematic review suggests damage to the STP is associated with CPSP and this could provide insights into mechanisms and treatment. Moreover, historical connection of strokes in the thalamic region and CPSP should be reevaluated as many studies noted that strokes in other regions of the brain also produce CPSP.

Role of the caudal fastigial nucleus in saccade generation. II. Effects of muscimol inactivation

1993 ◽  
Vol 70 (5) ◽  
pp. 1741-1758 ◽  
Author(s):  
F. R. Robinson ◽  
A. Straube ◽  
A. F. Fuchs
Keyword(s):  
Brain Stem ◽  
Rhesus Macaques ◽  
Fastigial Nucleus ◽  
Gamma Aminobutyric Acid ◽  
End Points ◽  
Acceleration And Deceleration ◽  
Corrective Saccades ◽  
Corrective Saccade ◽  
The Right ◽  
The Brain

1. We studied the effect of temporarily inhibiting neurons in the caudal fastigial nucleus in two rhesus macaques trained to make saccades to jumping targets. We placed injections of the gamma-aminobutyric acid (GABA) agonist muscimol unilaterally or bilaterally at sites in the caudal fastigial nucleus where we had recorded saccade-related neurons a few minutes earlier. 2. Unilateral injections (n = 9) made horizontal saccades to the injected side hypermetric and those to the other side hypometric (mean gain of 1.37 and 0.61, respectively, for 10 degrees target steps, and 1.26 and 0.81 for 20 degrees target steps; normal saccade gain was 0.96). Saccades to vertical targets showed a small but significant hypermetria and curved strongly toward the side of the injection. The trajectories and end points of all targeted saccades were more variable than normal. 3. After unilateral injections, centripetal saccades were slightly larger than centrifugal saccades (mean gains for ipsilateral saccades were 1.42 and 1.31, respectively, for 10 degrees target steps, and 1.37 and 1.15 for 20 degrees target steps). 4. Unilateral injections increased the average acceleration of ipsilateral saccades and decreased the acceleration of contralateral saccades. Injections decreased both the acceleration and deceleration of vertical saccades. 5. After dysmetric saccades, monkeys acquired the target with an abnormally high number of hypometric corrective saccades. Injection increased the average number of corrective saccades from 0.6 to 2.1 after 10 degrees horizontal target steps and from 0.8 to 2.1 after 20 degrees steps. The size of each successive corrective saccade in a series decreased, and the latency from the previous corrective saccade increased. 6. Bilateral injections (n = 2) of muscimol, in which we injected first into the left caudal fastigial nucleus and then, within 30 min, into the right, made all saccades hypermetric (mean gain for 10 degrees right, left, up, and down saccades was 1.18, 1.49, 1.43, and 1.10, respectively). Paradoxically, bilateral injection decreased both saccade acceleration and deceleration. Saccade trajectories and end points were more variable than normal. 7. To account for the effects of our injections, we propose that the activity of caudal fastigial neurons on one side normally helps to decelerate ipsilateral saccades and helps to accelerate contralateral saccades by influencing the feedback loop of the saccade burst generator in the brain stem. Without caudal fastigial activity the brain stem burst generator produces hypermetric, variable saccades. We therefore also propose that the influence of caudal fastigial neurons on the burst generator makes saccades more consistent and accurate.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Inducing Implicit Arguments from Comparable Texts: A Framework and Its Applications

2015 ◽  
Vol 41 (4) ◽  
pp. 625-664 ◽  
Author(s):  
Michael Roth ◽  
Anette Frank
Keyword(s):  
Computational Models ◽  
Current Model ◽  
Implicit Argument ◽  
Implicit Arguments ◽  
Argument Realization ◽  
Projection Approach ◽  
Implicit And Explicit ◽  
Graph Based Model ◽  
A Current ◽  
Sentential Meaning

In this article, we investigate aspects of sentential meaning that are not expressed in local predicate–argument structures. In particular, we examine instances of semantic arguments that are only inferable from discourse context. The goal of this work is to automatically acquire and process such instances, which we also refer to as implicit arguments, to improve computational models of language. As contributions towards this goal, we establish an effective framework for the difficult task of inducing implicit arguments and their antecedents in discourse and empirically demonstrate the importance of modeling this phenomenon in discourse-level tasks. Our framework builds upon a novel projection approach that allows for the accurate detection of implicit arguments by aligning and comparing predicate–argument structures across pairs of comparable texts. As part of this framework, we develop a graph-based model for predicate alignment that significantly outperforms previous approaches. Based on such alignments, we show that implicit argument instances can be automatically induced and applied to improve a current model of linking implicit arguments in discourse. We further validate that decisions on argument realization, although being a subtle phenomenon most of the time, can considerably affect the perceived coherence of a text. Our experiments reveal that previous models of coherence are not able to predict this impact. Consequently, we develop a novel coherence model, which learns to accurately predict argument realization based on automatically aligned pairs of implicit and explicit arguments.

Substrate specificity and acute regulation of the tumour suppressor phosphatase, PTEN

2007 ◽  
Vol 74 ◽  
pp. 69-80 ◽  
Author(s):  
C. Peter Downes ◽  
Nevin Perera ◽  
Sarah Ross ◽  
Nick R. Leslie
Keyword(s):  
Protein Phosphatase ◽  
Current Model ◽  
Tumour Suppressor ◽  
Protein Substrates ◽  
Dual Specificity ◽  
Survival And Growth ◽  
Phosphoinositide 3 Kinase ◽  
Phosphatase And Tensin Homologue ◽  
A Current ◽  
Inhibit Cell Proliferation

PTEN (phosphatase and tensin homologue deleted on chromosome 10) is a tumour suppressor that functions as a PtdIns(3,4,5)P3 3-phosphatase to inhibit cell proliferation, survival and growth by antagonizing PI3K (phosphoinositide 3-kinase)-dependent signalling. Recent work has begun to focus attention on potential biological functions of the protein phosphatase activity of PTEN and on the possibility that some of its functions are phosphatase-independent. We discuss here the structural and regulatory mechanisms that account for the remarkable specificity of PTEN with respect to its PtdIns substrates and how it avoids the soluble headgroups of PtdIns that occur commonly in cells. Secondly we discuss the concept of PTEN as a constitutively active enzyme that is subject to negative regulation both physiologically and pathologically. Thirdly, we review the evidence that PTEN functions as a dual specificity phosphatase with discrete lipid and protein substrates. Lastly we present a current model of how PTEN may participate in the control of cell migration.

A Trial of Transcranial Polarization in Chronic Schizophrenics

1968 ◽  
Vol 114 (510) ◽  
pp. 635-637 ◽  
Author(s):  
Kenneth Lifshitz ◽  
Patrick Harper
Keyword(s):  
Controlled Trial ◽  
Current Level ◽  
Favourable Effect ◽  
Considerable Evidence ◽  
Chronic Schizophrenics ◽  
Number Of Patients ◽  
Schizophrenic Patients ◽  
Positive Polarization ◽  
The Brain ◽  
A Current

Considerable evidence has accumulated that alterations in the direct current fields of the brain can produce alterations in function (O'Leary and Goldring, 1964). In view of this a group of investigators instituted a clinical trial of the possible usefulness of transcranial polarization (Lippold and Redfearn, 1964; Redfearn et al., 1964; Costain et al., 1964). In the approach used a current was passed between electrodes attached just superior to the eyebrows and an electrode on the leg. The principal changes reported consisted of an elevation of mood and an increase in involvement with the environment when the head was positive relatively to the leg and a withdrawal and quietness when the head was negative relatively to the leg. The current level reported as effective was generally of the order of 250 microamperes. Among Lippold and Redfearn's subjects were seven schizophrenics, in six of whom brief D.C. polarization produced the expected effects. Among the subjects of Redfearn et al. were four schizophrenics, in all of whom some favourable effect from D.C. head positive polarization was reported. This study was uncontrolled. In a blind controlled trial, Costain et al. found head-positive polarization to be of therapeutic efficacy in a group of 24 depressed patients. Their interpretation of results was challenged by Dawson and Montagu (1965). In view of these reports, we decided that a pilot study of the possible efficacy of transcranial polarization in altering the non-responsive state of chronic schizophrenic patients was warranted. It was decided that a more longitudinal study would be of greater value in determining possible therapeutic usefulness than a shorter trial on a larger number of patients. The experiment was conducted on one of the research wards of Rockland State Hospital.

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