Modification of the projection from the sensory cortex to the motor cortex following the elimination of thalamic projections to the motor cortex in cats |
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| Authors: | H. Asanuma E. Kosar N. Tsukahara H. Robinson |
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| Affiliation: | 1. First Department of Neurology, Faculty of Medicine, Masaryk University and University Hospital of St. Anne, Brno, Czech Republic;2. Department of Neurology, Charles University Faculty of Medicine, Hradec Králové, Czech Republic;3. Department of Neurology, Faculty of Medicine, Masaryk University and University Hospital Brno, Brno, Czech Republic;4. Department of Statistical Modelling, Institute of Computer Science of the Czech Academy of Sciences, Prague, Czech Republic;5. Center for Magnetic Resonance Research (CMRR), University of Minnesota, Minneapolis, MN, United States of America;6. Central European Institute of Technology (CEITEC) Masaryk University, Neuroscience Centre, Brno, Czech Republic;7. Department of Neurology, Comprehensive Stroke Center, University Hospital Hradec Králové, Czech Republic;8. Department of Neurology, Charles University, First Faculty of Medicine and General University Hospital, Prague, Czech Republic;1. McConnell Brain Imaging Centre, Montreal Neurological Institute and Hospital, McGill University, Montreal, QC, Canada;2. Department of Data Science, Inha University, Incheon, South Korea;3. Department of Statistics and Data Science, Inha University, Incheon, South Korea;4. Center for Neuroscience Imaging Research, Institute for Basic Science, Suwon, South Korea;5. Convergence Research Institute, Sungkyunkwan University, Suwon, South Korea;6. Center for the Developing Brain, Child Mind Institute, New York, United States;7. Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany;8. Department of Biomedical Engineering, Sungkyunkwan University, Suwon, South Korea |
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| Abstract: | ![]()
Examination of the projection from area 2 of the sensory cortex to the motor cortex revealed substantial changes following lesion of the ventrolateral nucleus of the thalamus. These observed changes were as follows. (1) The polarity of the evoked potentials elicited by area 2 stimulation reversed in the depth of the motor cortex whereas in normal animals, there was no reversal. (2) The amplitude of area 2-elicited EPSPs in the motor cortical neurons became greater following the lesion of VL. (3) The shape of the observed EPSPs was characterized by multiple peaks whereas in normal animals, the EPSPs were generally smooth and monophasic. (4) Neurons receiving a short-latency input from area 2 were distributed throughout the depths of the motor cortex whereas in normal animals, they were located only in the upper layers (layers II and III). (5) Intracellular injection of HRP revealed that the neurons receiving short-latency input were not restricted to typical stellate type cells, but also included bipolar or bitufted neurons with elongated cell bodies and polarized arborizations. These neurons were located in the superficial (II and III) as well as in the deep (V) layer. It is concluded that the elimination of thalamic input resulted in the reinforcement of the corticocortical input to the motor cortex. The subsequently observed corticocortical projection extended to neurons did not originally innervated by the association fibers. The results suggested that functional recovery following thalamic lesion is partly due to reorganization of projections from the sensory cortex to the motor cortex. |
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| Keywords: | motor cortex sensory cortex ventrolateral thalamus association fiber thalamocortical projection |
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