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001     156530
005     20220930130033.0
024 7 _ |a 10.3389/fnana.2014.00115
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037 _ _ |a FZJ-2014-05244
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Butz, Markus
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245 _ _ |a Homeostatic structural plasticity can account for topology changes following deafferentation and focal stroke
260 _ _ |a Lausanne
|c 2014
|b Frontiers Research Foundation
336 7 _ |a article
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336 7 _ |a ARTICLE
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520 _ _ |a After brain lesions caused by tumors or stroke, or after lasting loss of input (deafferentation), inter- and intra-regional brain networks respond with complex changes in topology. Not only areas directly affected by the lesion but also regions remote from the lesion may alter their connectivity—a phenomenon known as diaschisis. Changes in network topology after brain lesions can lead to cognitive decline and increasing functional disability. However, the principles governing changes in network topology are poorly understood. Here, we investigated whether homeostatic structural plasticity can account for changes in network topology after deafferentation and brain lesions. Homeostatic structural plasticity postulates that neurons aim to maintain a desired level of electrical activity by deleting synapses when neuronal activity is too high and by providing new synaptic contacts when activity is too low. Using our Model of Structural Plasticity, we explored how local changes in connectivity induced by a focal loss of input affected global network topology. In accordance with experimental and clinical data, we found that after partial deafferentation, the network as a whole became more random, although it maintained its small-world topology, while deafferentated neurons increased their betweenness centrality as they rewired and returned to the homeostatic range of activity. Furthermore, deafferentated neurons increased their global but decreased their local efficiency and got longer tailed degree distributions, indicating the emergence of hub neurons. Together, our results suggest that homeostatic structural plasticity may be an important driving force for lesion-induced network reorganization and that the increase in betweenness centrality of deafferentated areas may hold as a biomarker for brain repair.
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588 _ _ |a Dataset connected to CrossRef, juser.fz-juelich.de
700 1 _ |a Steenbuck, Ines D.
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700 1 _ |a van Ooyen, Arjen
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770 _ _ |a Quantitative analysis of neuroanatomy
773 _ _ |a 10.3389/fnana.2014.00115
|g Vol. 8
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|p 115
|t Frontiers in neuroanatomy
|v 8
|y 2014
|x 1662-5129
856 4 _ |u http://journal.frontiersin.org/Journal/10.3389/fnana.2014.00115/abstract
856 4 _ |u https://juser.fz-juelich.de/record/156530/files/FZJ-2014-05244.pdf
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910 1 _ |a Forschungszentrum Jülich GmbH
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914 1 _ |y 2014
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