% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Butz:156530,
author = {Butz, Markus and Steenbuck, Ines D. and van Ooyen, Arjen},
title = {{H}omeostatic structural plasticity can account for
topology changes following deafferentation and focal stroke},
journal = {Frontiers in neuroanatomy},
volume = {8},
issn = {1662-5129},
address = {Lausanne},
publisher = {Frontiers Research Foundation},
reportid = {FZJ-2014-05244},
pages = {115},
year = {2014},
abstract = {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.},
cin = {JSC / JARA-HPC},
ddc = {610},
cid = {I:(DE-Juel1)JSC-20090406 / $I:(DE-82)080012_20140620$},
pnm = {411 - Computational Science and Mathematical Methods
(POF2-411) / SMHB - Supercomputing and Modelling for the
Human Brain (HGF-SMHB-2013-2017) / SLNS - SimLab
Neuroscience (Helmholtz-SLNS)},
pid = {G:(DE-HGF)POF2-411 / G:(DE-Juel1)HGF-SMHB-2013-2017 /
G:(DE-Juel1)Helmholtz-SLNS},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000344069100001},
doi = {10.3389/fnana.2014.00115},
url = {https://juser.fz-juelich.de/record/156530},
}