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      Discrimination of Motion Direction in a Robot Using a Phenomenological Model of Synaptic Plasticity

      research-article
      , ,
      Computational Intelligence and Neuroscience
      Hindawi

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          Abstract

          Recognizing and tracking the direction of moving stimuli is crucial to the control of much animal behaviour. In this study, we examine whether a bio-inspired model of synaptic plasticity implemented in a robotic agent may allow the discrimination of motion direction of real-world stimuli. Starting with a well-established model of short-term synaptic plasticity (STP), we develop a microcircuit motif of spiking neurons capable of exhibiting preferential and nonpreferential responses to changes in the direction of an orientation stimulus in motion. While the robotic agent processes sensory inputs, the STP mechanism introduces direction-dependent changes in the synaptic connections of the microcircuit, resulting in a population of units that exhibit a typical cortical response property observed in primary visual cortex (V1), namely, direction selectivity. Visually evoked responses from the model are then compared to those observed in multielectrode recordings from V1 in anesthetized macaque monkeys, while sinusoidal gratings are displayed on a screen. Overall, the model highlights the role of STP as a complementary mechanism in explaining the direction selectivity and applies these insights in a physical robot as a method for validating important response characteristics observed in experimental data from V1, namely, direction selectivity.

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          Most cited references59

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          Short-term synaptic plasticity.

          Synaptic transmission is a dynamic process. Postsynaptic responses wax and wane as presynaptic activity evolves. This prominent characteristic of chemical synaptic transmission is a crucial determinant of the response properties of synapses and, in turn, of the stimulus properties selected by neural networks and of the patterns of activity generated by those networks. This review focuses on synaptic changes that result from prior activity in the synapse under study, and is restricted to short-term effects that last for at most a few minutes. Forms of synaptic enhancement, such as facilitation, augmentation, and post-tetanic potentiation, are usually attributed to effects of a residual elevation in presynaptic [Ca(2+)]i, acting on one or more molecular targets that appear to be distinct from the secretory trigger responsible for fast exocytosis and phasic release of transmitter to single action potentials. We discuss the evidence for this hypothesis, and the origins of the different kinetic phases of synaptic enhancement, as well as the interpretation of statistical changes in transmitter release and roles played by other factors such as alterations in presynaptic Ca(2+) influx or postsynaptic levels of [Ca(2+)]i. Synaptic depression dominates enhancement at many synapses. Depression is usually attributed to depletion of some pool of readily releasable vesicles, and various forms of the depletion model are discussed. Depression can also arise from feedback activation of presynaptic receptors and from postsynaptic processes such as receptor desensitization. In addition, glial-neuronal interactions can contribute to short-term synaptic plasticity. Finally, we summarize the recent literature on putative molecular players in synaptic plasticity and the effects of genetic manipulations and other modulatory influences.
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            Noise in the nervous system.

            Noise--random disturbances of signals--poses a fundamental problem for information processing and affects all aspects of nervous-system function. However, the nature, amount and impact of noise in the nervous system have only recently been addressed in a quantitative manner. Experimental and computational methods have shown that multiple noise sources contribute to cellular and behavioural trial-to-trial variability. We review the sources of noise in the nervous system, from the molecular to the behavioural level, and show how noise contributes to trial-to-trial variability. We highlight how noise affects neuronal networks and the principles the nervous system applies to counter detrimental effects of noise, and briefly discuss noise's potential benefits.
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              Regulation of synaptic efficacy by coincidence of postsynaptic APs and EPSPs.

              Activity-driven modifications in synaptic connections between neurons in the neocortex may occur during development and learning. In dual whole-cell voltage recordings from pyramidal neurons, the coincidence of postsynaptic action potentials (APs) and unitary excitatory postsynaptic potentials (EPSPs) was found to induce changes in EPSPs. Their average amplitudes were differentially up- or down-regulated, depending on the precise timing of postsynaptic APs relative to EPSPs. These observations suggest that APs propagating back into dendrites serve to modify single active synaptic connections, depending on the pattern of electrical activity in the pre- and postsynaptic neurons.
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                Author and article information

                Contributors
                Journal
                Comput Intell Neurosci
                Comput Intell Neurosci
                CIN
                Computational Intelligence and Neuroscience
                Hindawi
                1687-5265
                1687-5273
                2019
                2 May 2019
                : 2019
                : 6989128
                Affiliations
                Laboratory for Computational Neurodynamics and Cognition, School of Psychology, University of Ottawa, Ottawa, ON, Canada K1N 6N5
                Author notes

                Guest Editor: Uma Seeboonruang

                Author information
                http://orcid.org/0000-0003-3067-9432
                Article
                10.1155/2019/6989128
                6525956
                51b54a1b-42c9-47f4-baf4-e6191c0eab9d
                Copyright © 2019 Nareg Berberian et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 12 October 2018
                : 14 February 2019
                : 19 March 2019
                Funding
                Funded by: Natural Sciences and Engineering Research Council of Canada
                Award ID: 210663
                Funded by: Ontario Graduate Scholarship
                Categories
                Research Article

                Neurosciences
                Neurosciences

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