scholarly journals Sensorimotor adaptation error signals are derived from realistic predictions of movement outcomes

2011 ◽  
Vol 105 (3) ◽  
pp. 1130-1140 ◽  
Author(s):  
Aaron L. Wong ◽  
Mark Shelhamer
Keyword(s):  
Human Subjects ◽  
Motor Command ◽  
Neural Systems ◽  
Error Signal ◽  
The Difference ◽  
Motor Outcomes ◽  
Saccade Adaptation ◽  
Visual Error ◽  
Realistic Prediction ◽  
Adaptation Task

Neural systems that control movement maintain accuracy by adaptively altering motor commands in response to errors. It is often assumed that the error signal that drives adaptation is equivalent to the sensory error observed at the conclusion of a movement; for saccades, this is typically the visual (retinal) error. However, we instead propose that the adaptation error signal is derived as the difference between the observed visual error and a realistic prediction of movement outcome. Using a modified saccade-adaptation task in human subjects, we precisely controlled the amount of error experienced at the conclusion of a movement by back-stepping the target so that the saccade is hypometric (positive retinal error), but less hypometric than if the target had not moved (smaller retinal error than expected). This separates prediction error from both visual errors and motor corrections. Despite positive visual errors and forward-directed motor corrections, we found an adaptive decrease in saccade amplitudes, a finding that is well-explained by the employment of a prediction-based error signal. Furthermore, adaptive changes in movement size were linearly correlated to the disparity between the predicted and observed movement outcomes, in agreement with the forward-model hypothesis of motor learning, which states that adaptation error signals incorporate predictions of motor outcomes computed using a copy of the motor command (efference copy).

Effect of Visual Error Size on Saccade Adaptation in Monkey

2003 ◽  
Vol 90 (2) ◽  
pp. 1235-1244 ◽  
Author(s):  
Farrel R. Robinson ◽  
Christopher T. Noto ◽  
Scott E. Bevans
Keyword(s):  
Eye Position ◽  
Error Signal ◽  
Target Movement ◽  
Target Eccentricity ◽  
Saccade Size ◽  
Saccade Adaptation ◽  
Visual Error ◽  
The Relationship ◽  
Initial Target ◽  
Gain Change

Saccades that consistently over- or undershoot their targets gradually become smaller or larger, respectively. The signal that elicits adaptation of saccade size is a difference between eye and target positions appearing repeatedly at the ends of saccades. Here we describe how visual error size affects the size of saccade adaptation. At the end of each saccade, we imposed a constant-sized error by moving the target to a specified point relative to eye position. We tested a variety of error sizes imposed after saccades to target movements of 6, 12, and 18°. We found that the size of the gain change elicited in a particular experiment depended on both the size of the imposed postsaccade error and on the size of the preceding target movement. For example, imposed errors of 4–5° reduce saccades tracking 6, 12, and 18° target movements by an average of 18, 35, and 45%, respectively. The most effective errors were those that were 15–45% of the size of the initial target eccentricity. Negative errors, which reduce saccade size, were more effective in changing saccade gain than were positive errors, which increased saccade size. For example, for 12° target movements, negative and positive errors of 2–6° changed saccade gain an average of 35 and 8%, respectively. This description of the relationship between error size and adaptation size improves our ability to adapt saccades in the laboratory and characterizes the error sizes that will best drive neurons carrying the adaptation-related visual error signal.

scholarly journals Modification of saccadic gain by reinforcement

2011 ◽  
Vol 106 (1) ◽  
pp. 219-232 ◽  
Author(s):  
Laurent Madelain ◽  
Céline Paeye ◽  
Josh Wallman
Keyword(s):  
Target Location ◽  
Error Signal ◽  
Saccade Amplitude ◽  
Learning Mechanisms ◽  
Progressive Change ◽  
Compensatory Process ◽  
Amplitude Criterion ◽  
Original Target ◽  
Saccade Adaptation ◽  
Visual Error

Control of saccadic gain is often viewed as a simple compensatory process in which gain is adjusted over many trials by the postsaccadic retinal error, thereby maintaining saccadic accuracy. Here, we propose that gain might also be changed by a reinforcement process not requiring a visual error. To test this hypothesis, we used experimental paradigms in which retinal error was removed by extinguishing the target at the start of each saccade and either an auditory tone or the vision of the target on the fovea was provided as reinforcement after those saccades that met an amplitude criterion. These reinforcement procedures caused a progressive change in saccade amplitude in nearly all subjects, although the rate of adaptation differed greatly among subjects. When we reversed the contingencies and reinforced those saccades landing closer to the original target location, saccade gain changed back toward normal gain in most subjects. When subjects had saccades adapted first by reinforcement and a week later by conventional intrasaccadic step adaptation, both paradigms yielded similar degrees of gain changes and similar transfer to new amplitudes and to new starting positions of the target step as well as comparable rates of recovery. We interpret these changes in saccadic gain in the absence of postsaccadic retinal error as showing that saccade adaptation is not controlled by a single error signal. More generally, our findings suggest that normal saccade adaptation might involve general learning mechanisms rather than only specialized mechanisms for motor calibration.

scholarly journals The Effect of Visual Uncertainty on Implicit Motor Adaptation

2020 ◽  
Author(s):  
Jonathan S. Tsay ◽  
Guy Avraham ◽  
Hyosub E. Kim ◽  
Darius E. Parvin ◽  
Zixuan Wang ◽  
...  
Keyword(s):  
Alternative Hypothesis ◽  
Visuomotor Adaptation ◽  
Modular System ◽  
Feedback Signal ◽  
Sensorimotor Adaptation ◽  
Prediction Errors ◽  
Error Signal ◽  
The Difference ◽  
Visual Error ◽  
Sensorimotor Map

ABSTRACTSensorimotor adaptation is driven by sensory prediction errors, the difference between the predicted and actual feedback. When the position of the feedback is made uncertain, adaptation is attenuated. This effect, in the context of optimal sensory integration models, has been attributed to a weakening of the error signal driving adaptation. Here we consider an alternative hypothesis, namely that uncertainty alters the perceived location of the feedback. We present two visuomotor adaptation experiments to compare these hypotheses, varying the size and uncertainty of a visual error signal. Uncertainty attenuated learning when the error size was small but had no effect when the error size was large. This pattern of results favors the hypothesis that uncertainty does not impact the strength of the error signal, but rather, leads to mis-localization of the error. We formalize these ideas to offer a novel perspective on the effect of visual uncertainty on implicit sensorimotor adaptation.SIGNIFICANCE STATEMENTCurrent models of sensorimotor adaptation assume that the rate of learning will be related to properties of the error signal (e.g., size, consistency, relevance). Recent evidence has challenged this view, pointing to a rigid, modular system, one that automatically recalibrates the sensorimotor map in response to movement errors, with minimal constraint. In light of these developments, this study revisits the influence of feedback uncertainty on sensorimotor adaptation. Adaptation was attenuated in response to a noisy feedback signal, but the effect was only manifest for small errors and not for large errors. This interaction suggests that uncertainty does not weaken the error signal. Rather, it may influence the perceived location of the feedback and thus the change in the sensorimotor map induced by that error. These ideas are formalized to show how the motor system remains exquisitely calibrated, even if adaptation is largely insensitive to the statistics of error signals.

Mislocalization of stationary and flashed bars after saccadic inward and outward adaptation of reactive saccades

2012 ◽  
Vol 107 (11) ◽  
pp. 3062-3070 ◽  
Author(s):  
Fabian Schnier ◽  
Markus Lappe
Keyword(s):  
Saccade Target ◽  
Saccade Amplitude ◽  
Presentation Duration ◽  
Target Presentation ◽  
Adaptation Mechanisms ◽  
Long Duration ◽  
Neuronal Mechanisms ◽  
The Difference ◽  
Saccade Adaptation

Recent studies have shown that saccadic inward adaptation (i.e., the shortening of saccade amplitude) and saccadic outward adaptation (i.e., the lengthening of saccade amplitude) rely on partially different neuronal mechanisms. There is increasing evidence that these differences are based on differences at the target registration or planning stages since outward but not inward adaptation transfers to hand-pointing and perceptual localization of flashed targets. Furthermore, the transfer of reactive saccade adaptation to long-duration overlap and scanning saccades is stronger after saccadic outward adaptation than that after saccadic inward adaptation, suggesting that modulated target registration stages during outward adaptation are increasingly used in the execution of saccades when the saccade target is visually available for a longer time. The difference in target presentation duration between reactive and scanning saccades is also linked to a difference in perceptual localization of different targets. Flashed targets are mislocalized after inward adaptation of reactive and scanning saccades but targets that are presented for a longer time (stationary targets) are mislocalized stronger after scanning than after reactive saccades. This link between perceptual localization and adaptation specificity suggests that mislocalization of stationary bars should be higher after outward than that after inward adaptation of reactive saccades. In the present study we test this prediction. We show that the relative amount of mislocalization of stationary versus flashed bars is higher after outward than that after inward adaptation of reactive saccades. Furthermore, during fixation stationary and flashed bars were mislocalized after outward but not after inward adaptation. Thus, our results give further evidence for different adaptation mechanisms between inward and outward adaptation and harmonize some recent research.

STUDIES ON HABITUATION TO COLD PAIN

1966 ◽  
Vol 44 (2) ◽  
pp. 287-293 ◽  
Author(s):  
Jacques LeBlanc ◽  
Pierre Potvin
Keyword(s):  
Cold Water ◽  
Mental Arithmetic ◽  
Blood Pressure Response ◽  
Human Subjects ◽  
Cold Pain ◽  
Left Hand ◽  
Water Test ◽  
The Difference ◽  
The Right ◽  
Habituation To Cold

It was possible to produce habituation to cold in a group of human subjects by immersing the left hand in cold water for [Formula: see text] minutes twice a day for 19 days. The right hand did not adapt. Another group of subjects was exposed similarly with the difference that an anxiety test (mental arithmetic test) was always given simultaneously with the cold-water test. In this second group the original blood pressure response, i.e. for the first day, was greater than in the first group because of the cumulative effects of the two tests. After 19 days definite evidence was obtained for adaptation to these two tests administered together. However, when these tests were given separately to the second group, no adaptation was evident; adaptation occurred only to both tests given simultaneously. These results indicate that no adaptation develops to cold per se if the subjects are distracted from cold discomfort. It was also found that adaptation of one hand to cold water not only failed to induce adaptation in the opposite hand but even reinforced responses of the unadapted hand. These findings suggest a participation of the central nervous system in adaptation to cold pain, and tend to minimize the importance of local peripheral changes.

Saccadic Gain Modification: Visual Error Drives Motor Adaptation

1998 ◽  
Vol 80 (5) ◽  
pp. 2405-2416 ◽  
Author(s):  
Josh Wallman ◽  
Albert F. Fuchs
Keyword(s):  
Target Location ◽  
Rhesus Macaques ◽  
Motor Adaptation ◽  
Saccadic Eye Movements ◽  
Target Distance ◽  
Error Signal ◽  
Gain Adaptation ◽  
Horizontal Saccade ◽  
Corrective Saccades ◽  
Visual Error

Wallman, Josh and Albert F. Fuchs. Saccadic gain modification: visual error drives motor adaptation. J. Neurophysiol. 80: 2405–2416, 1998. The brain maintains the accuracy of saccadic eye movements by adjusting saccadic amplitude relative to the target distance (i.e., saccade gain) on the basis of the performance of recent saccades. If an experimenter surreptitiously moves the target backward during each saccade, thereby causing the eyes to land beyond their targets, saccades undergo a gradual gain reduction. The error signal driving this conventional saccadic gain adaptation could be either visual (the postsaccadic distance of the target from the fovea) or motoric (the direction and size of the corrective saccade that brings the eye onto the back-stepped target). Similarly, the adaptation itself might be a motor adjustment (change in the size of saccade for a given perceived target distance) or a visual remapping (change in the perceived target distance). We studied these possibilities in experiments both with rhesus macaques and with humans. To test whether the error signal is motoric, we used a paradigm devised by Heiner Deubel. The Deubel paradigm differed from the conventional adaptation paradigm in that the backward step that occurred during the saccade was brief, and the target then returned to its original displaced location. This ploy replaced most of the usual backward corrective saccades with forward ones. Nevertheless, saccadic gain gradually decreased over hundreds of trials. Therefore, we conclude that the direction of saccadic gain adaptation is not determined by the direction of corrective saccades. To test whether gain adaptation is a manifestation of a static visual remapping, we decreased the gain of 10° horizontal saccades by conventional adaptation and then tested the gain to targets appearing at retinal locations unused during adaptation. To make the target appear in such “virgin territory,” we had it jump first vertically and then 10° horizontally; both jumps were completed and the target spot extinguished before saccades were made sequentially to the remembered target locations. Conventional adaptation decreased the gain of the second, horizontal saccade even though the target was in a nonadapted retinal location. In contrast, the horizontal component of oblique saccades made directly to the same virgin location showed much less gain decrease, suggesting that the adaptation is specific to saccade direction rather than to target location. Thus visual remapping cannot account for the entire reduction of saccadic gain. We conclude that saccadic gain adaptation involves an error signal that is primarily visual, not motor, but that the adaptation itself is primarily motor, not visual.

Effect of visual error manipulation on saccade adaptation

2011 ◽  
Vol 71 ◽  
pp. e143
Author(s):  
Yukinori Yamashita ◽  
Yuki Kaku ◽  
Kaoru Yoshida ◽  
Yoshiki Iwamoto
Keyword(s):  
Saccade Adaptation ◽  
Visual Error

scholarly journals Reconstruction of input functions from a dynamic PET image with sequential administration of 15O2 and H215O for noninvasive and ultra-rapid measurement of CBF, OEF, and CMRO2

2017 ◽  
Vol 38 (5) ◽  
pp. 780-792 ◽  
Author(s):  
Nobuyuki Kudomi ◽  
Yukito Maeda ◽  
Hiroyuki Yamamoto ◽  
Yuka Yamamoto ◽  
Tetsuhiro Hatakeyama ◽  
...  
Keyword(s):  
Rate Constants ◽  
Human Subjects ◽  
Invasive Procedure ◽  
Invasive Technique ◽  
Invasive Approach ◽  
Non Invasive ◽  
Sequential Administration ◽  
Invasive Method ◽  
The Difference ◽  
Arterial Input Functions

CBF, OEF, and CMRO2 images can be quantitatively assessed using PET. Their image calculation requires arterial input functions, which require invasive procedure. The aim of the present study was to develop a non-invasive approach with image-derived input functions (IDIFs) using an image from an ultra-rapid O2 and C15O2 protocol. Our technique consists of using a formula to express the input using tissue curve with rate constants. For multiple tissue curves, the rate constants were estimated so as to minimize the differences of the inputs using the multiple tissue curves. The estimated rates were used to express the inputs and the mean of the estimated inputs was used as an IDIF. The method was tested in human subjects ( n = 24). The estimated IDIFs were well-reproduced against the measured ones. The difference in the calculated CBF, OEF, and CMRO2 values by the two methods was small (<10%) against the invasive method, and the values showed tight correlations ( r = 0.97). The simulation showed errors associated with the assumed parameters were less than ∼10%. Our results demonstrate that IDIFs can be reconstructed from tissue curves, suggesting the possibility of using a non-invasive technique to assess CBF, OEF, and CMRO2.

scholarly journals Silence, Solitude, and Serotonin: Neural Mechanisms Linking Hearing Loss and Social Isolation

2020 ◽  
Vol 10 (6) ◽  
pp. 367
Author(s):  
Sarah M. Keesom ◽  
Laura M. Hurley
Keyword(s):  
Hearing Loss ◽  
Social Isolation ◽  
Human Subjects ◽  
Brain Regions ◽  
Neural Systems ◽  
Depression And Anxiety ◽  
Auditory Cognition ◽  
Regulatory Systems ◽  
Two Factors ◽  
And Function

For social animals that communicate acoustically, hearing loss and social isolation are factors that independently influence social behavior. In human subjects, hearing loss may also contribute to objective and subjective measures of social isolation. Although the behavioral relationship between hearing loss and social isolation is evident, there is little understanding of their interdependence at the level of neural systems. Separate lines of research have shown that social isolation and hearing loss independently target the serotonergic system in the rodent brain. These two factors affect both presynaptic and postsynaptic measures of serotonergic anatomy and function, highlighting the sensitivity of serotonergic pathways to both types of insult. The effects of deficits in both acoustic and social inputs are seen not only within the auditory system, but also in other brain regions, suggesting relatively extensive effects of these deficits on serotonergic regulatory systems. Serotonin plays a much-studied role in depression and anxiety, and may also influence several aspects of auditory cognition, including auditory attention and understanding speech in challenging listening conditions. These commonalities suggest that serotonergic pathways are worthy of further exploration as potential intervening mechanisms between the related conditions of hearing loss and social isolation, and the affective and cognitive dysfunctions that follow.

scholarly journals Fermentation of non-starch polysaccharides in mixed diets and single fibre sources: comparative studies in human subjects andin vitro

1998 ◽  
Vol 80 (3) ◽  
pp. 253-261 ◽  
Author(s):  
Elisabeth Wisker ◽  
Martina Daniel ◽  
Gerhard Rave ◽  
Walter Feldheim
Keyword(s):  
Human Subjects ◽  
Single Fibre ◽  
Physiological Importance ◽  
Rye Bread ◽  
Batch System ◽  
The Difference ◽  
Mean Differences ◽  
Balance Trials

The present study investigated whether the extent of fermentation of NSP in human subjects could be predicted by anin vitrobatch system. Fibre sources studied were five mixed diets containing different amounts and types of fibre and three single fibre sources (citrus fibre concentrate, coarse and fine wholemeal rye bread). Fermentation in human subjects was determined in balance experiments in women who were also donors of the faecal inocula.In vitrofermentations were performed with fibre residues prepared from duplicates of the fibre-containing foods consumed during the balance trials. Fermentation of total NSPin vivowas between 65.8 and 88.6% for the mixed diets and 54.4, 58.0 and 96.9 % for the coarse and fine wholemeal rye breads and the citrus fibre concentrate respectively. For the mixed diets and the citrus fibre concentrate, mean differences between the extent of NSP degradation after 24 hin vitroincubation and thatin vivowere between −0.7 and 5.0 %. Differences were significant for one diet (P< 0.05). For the wholemeal rye breads, the fermentationin vitroexceeded thatin vivosignificantly, but the magnitude of the difference in each case was small and without physiological importance. Particle size of breads had no influence on the extent of NSP degradation. These results indicate that thein vitrobatch system used could provide quantitative data on the fermentationin vivoof NSP in mixed diets and some single fibre sources. Anin vitroincubation time of 24 h was sufficient to mimic the NSP degradationin vivo.

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