41
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      The dissociable effects of punishment and reward on motor learning.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          A common assumption regarding error-based motor learning (motor adaptation) in humans is that its underlying mechanism is automatic and insensitive to reward- or punishment-based feedback. Contrary to this hypothesis, we show in a double dissociation that the two have independent effects on the learning and retention components of motor adaptation. Negative feedback, whether graded or binary, accelerated learning. While it was not necessary for the negative feedback to be coupled to monetary loss, it had to be clearly related to the actual performance on the preceding movement. Positive feedback did not speed up learning, but it increased retention of the motor memory when performance feedback was withdrawn. These findings reinforce the view that independent mechanisms underpin learning and retention in motor adaptation, reject the assumption that motor adaptation is independent of motivational feedback, and raise new questions regarding the neural basis of negative and positive motivational feedback in motor learning.

          Related collections

          Most cited references27

          • Record: found
          • Abstract: found
          • Article: not found

          A computational neuroanatomy for motor control.

          The study of patients to infer normal brain function has a long tradition in neurology and psychology. More recently, the motor system has been subject to quantitative and computational characterization. The purpose of this review is to argue that the lesion approach and theoretical motor control can mutually inform each other. Specifically, one may identify distinct motor control processes from computational models and map them onto specific deficits in patients. Here we review some of the impairments in motor control, motor learning and higher-order motor control in patients with lesions of the corticospinal tract, the cerebellum, parietal cortex, the basal ganglia, and the medial temporal lobe. We attempt to explain some of these impairments in terms of computational ideas such as state estimation, optimization, prediction, cost, and reward. We suggest that a function of the cerebellum is system identification: to build internal models that predict sensory outcome of motor commands and correct motor commands through internal feedback. A function of the parietal cortex is state estimation: to integrate the predicted proprioceptive and visual outcomes with sensory feedback to form a belief about how the commands affected the states of the body and the environment. A function of basal ganglia is related to optimal control: learning costs and rewards associated with sensory states and estimating the "cost-to-go" during execution of a motor task. Finally, functions of the primary and the premotor cortices are related to implementing the optimal control policy by transforming beliefs about proprioceptive and visual states, respectively, into motor commands.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Dynamic dopamine modulation in the basal ganglia: a neurocomputational account of cognitive deficits in medicated and nonmedicated Parkinsonism.

            Dopamine (DA) depletion in the basal ganglia (BG) of Parkinson's patients gives rise to both frontal-like and implicit learning impairments. Dopaminergic medication alleviates some cognitive deficits but impairs those that depend on intact areas of the BG, apparently due to DA ''overdose.'' These findings are difficult to accommodate with verbal theories of BG/DA function, owing to complexity of system dynamics: DA dynamically modulates function in the BG, which is itself a modulatory system. This article presents a neural network model that instantiates key biological properties and provides insight into the underlying role of DA in the BG during learning and execution of cognitive tasks. Specifically, the BG modulates the execution of ''actions'' (e.g., motor different parts of the frontal cortex. Phasic changes in DA, which occur during error feedback, dynamically modulate the BG threshold for facilitating/suppressing a cortical command in response to particular stimuli. Reduced dynamic range of DA explains Parkinson and DA overdose deficits with a single underlying dysfunction, despite overall differences in raw DA levels. Simulated Parkinsonism and medication effects provide a theoretical basis for behavioral data in probabilistic classification and reversal tasks. The model also provides novel testable predictions for neuropsychological and pharmacological studies, and motivates further investigation of BG/DA interactions with the prefrontal cortex in working memory.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Complementary roles of basal ganglia and cerebellum in learning and motor control.

              K Doya (2000)
              The classical notion that the basal ganglia and the cerebellum are dedicated to motor control has been challenged by the accumulation of evidence revealing their involvement in non-motor, cognitive functions. From a computational viewpoint, it has been suggested that the cerebellum, the basal ganglia, and the cerebral cortex are specialized for different types of learning: namely, supervised learning, reinforcement learning and unsupervised learning, respectively. This idea of learning-oriented specialization is helpful in understanding the complementary roles of the basal ganglia and the cerebellum in motor control and cognitive functions.
                Bookmark

                Author and article information

                Journal
                Nat. Neurosci.
                Nature neuroscience
                1546-1726
                1097-6256
                Apr 2015
                : 18
                : 4
                Affiliations
                [1 ] School of Psychology, University of Birmingham, Birmingham, UK.
                [2 ] Sobell Department for Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, UK.
                [3 ] Insititute of Cognitive Neuroscience, University College London, London, UK.
                Article
                nn.3956
                10.1038/nn.3956
                25706473
                a3d026e8-cf41-43a8-a9e7-dff1fd73f746
                History

                Comments

                Comment on this article