A Model of TMS-induced I-waves in Motor Cortex |
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| Institution: | 1. Frankfurt Institute for Advanced Studies, Frankfurt am Main, Germany;2. Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard Karls University, Tübingen, Germany;3. Center for Cognitive and Neural Studies (Coneural), Romanian Institute of Science and Technology, Cluj-Napoca, Romania;4. Department of Physics, Goethe University, Frankfurt am Main, Germany;5. Department of Computer Science, Babe?-Bolyai University, Cluj-Napoca, Romania;1. Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, NC, USA;2. Department of Psychology and Neuroscience, Duke University, USA;3. Department of Biomedical Engineering, Duke University, USA;4. Department of Electrical and Computer Engineering, Duke University, USA;1. Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark;2. Department of Neurosciences, Reproductive Sciences and Odontostomatology, University Federico II of Naples, Italy;3. INSERM, U1216, Grenoble Institut des Neurosciences, GIN, F-38000 Grenoble, France;4. Department of Electrical Engineering, Technical University of Denmark, Kongens Lyngby, Denmark;5. Department of Neurology, Copenhagen University Hospital Bispebjerg, Copenhagen, Denmark;1. Department of Clinical Neurophysiology, Kuopio University Hospital, Kuopio, Finland;2. Department of Applied Physics, University of Eastern Finland, Kuopio, Finland;3. A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland;4. Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, United States;5. Department of Neuroscience and Biomedical Engineering, Aalto University School of Science, Espoo, Finland;1. Institute of Neurology, Department of Geriatrics, Neuroscience and Orthopedics, Catholic University, Policlinic A. Gemelli, Rome, Italy;2. Department of Neurology, Royal Prince Alfred Hospital, University of Sydney, Sydney, Australia;3. Division of Neurology, Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada;4. Human Cortical Physiology and Neurorehabilitation Section, NINDS, NIH, Bethesda, MD, USA;5. Temerty Centre for Therapeutic Brain Intervention, Centre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada;6. Department of Neurology, University Campus Bio-medico, Rome, Italy;7. Department of Clinical Neurophysiology, University of Eastern Finland, Kuopio, Finland;8. Monash Alfred Psychiatry Research Centre, Monash University Central Clinical School and The Alfred, Melbourne, Australia;9. Medical University of South Carolina, Ralph H. Johnson VA Medical Center, Charleston, SC, USA;10. Human Motor Control Section, Medical Neurology Branch, NINDS, NIH, Bethesda, MD, USA;11. Department of Physiology, Henri Mondor Hospital, Assistance Publique – Hôpitaux de Paris, Créteil, France;12. EA 4391, Nerve Excitability and Therapeutic Team, Faculty of Medicine, Paris Est Créteil University, Créteil, France;13. Department of Psychiatry and Psychotherapy, University of Regensburg, Regensburg, Germany;14. Department of Neurology, Japanese Red Cross Medical Center, Tokyo, Japan;15. Department of Clinical and Experimental Sciences University of Brescia, Brescia, Italy;p. IRCCS Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy;q. Department of Clinical Neurophysiology, University Medical Center Göttingen, Georg-August-University, Göttingen, Germany;r. Berenson-Allen Center for Non-invasive Brain Stimulation, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA;s. Department of Clinical Neurophysiology, Georg-August University, Göttingen, Germany;t. Brain Investigation & Neuromodulation Lab, Unit of Neurology and Clinical Neurophysiology, Department of Neuroscience, University of Siena, Siena, Italy;u. Institute of Neurology, University College London, London, United Kingdom;v. Department of Neurology, Copenhagen University Hospital Bispebjerg, Copenhagen, Denmark;w. Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark;x. Department of Neurology, School of Medicine, Fukushima Medical University, Fukushima, Japan;y. Institute of Cognitive Neuroscience, University College London, London, United Kingdom;z. Department of Neurology & Stroke, and Hertie Institute for Clinical Brain Research, Eberhard Karls University, Tübingen, Germany;1. Faculty of Physical Therapy, Mahidol University, 73170 Nakonpathom, Thailand;2. UPMC Université Paris 06, CNRS, Inserm, laboratoire d’imagerie biomédicale, Sorbonne universités, 75013 Paris, France;3. Service de médecine physique et réadaptation, groupe hospitalier Pitié-Salpêtrière, AP–HP, France |
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| Abstract: | BackgroundTranscranial magnetic stimulation (TMS) allows to manipulate neural activity non-invasively, and much research is trying to exploit this ability in clinical and basic research settings. In a standard TMS paradigm, single-pulse stimulation over motor cortex produces repetitive responses in descending motor pathways called I-waves. However, the details of how TMS induces neural activity patterns in cortical circuits to produce these responses remain poorly understood. According to a traditional view, I-waves are due to repetitive synaptic inputs to pyramidal neurons in layer 5 (L5) of motor cortex, but the potential origin of such repetitive inputs is unclear.Objective/hypothesisHere we aim to test the plausibility of an alternative mechanism behind D- and I-wave generation through computational modeling. This mechanism relies on the broad distribution of conduction delays of synaptic inputs arriving at different parts of L5 cells' dendritic trees and their spike generation mechanism.MethodsOur model consists of a detailed L5 pyramidal cell and a population of layer 2 and 3 (L2/3) neurons projecting onto it with synapses exhibiting short-term depression. I-waves are simulated as superpositions of spike trains from a large population of L5 cells.ResultsOur model successfully reproduces all basic characteristics of I-waves observed in epidural responses during in vivo recordings of conscious humans. In addition, it shows how the complex morphology of L5 neurons might play an important role in the generation of I-waves. In the model, later I-waves are formed due to inputs to distal synapses, while earlier ones are driven by synapses closer to the soma. Finally, the model offers an explanation for the inhibition and facilitation effects in paired-pulse stimulation protocols.ConclusionsIn contrast to previous models, which required either neural oscillators or chains of inhibitory interneurons acting upon L5 cells, our model is fully feed-forward without lateral connections or loops. It parsimoniously explains findings from a range of experiments and should be considered as a viable alternative explanation of the generating mechanism of I-waves. |
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| Keywords: | Transcranial stimulation Motor cortex I-waves Computational model Neuron |
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