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@ARTICLE{Anders:267062,
author = {Anders, Stefanie and Breithausen, Björn and Unichenko,
Petr and Herde, Michel K and Minge, Daniel and Abramian,
Adlin and Behringer, Charlotte and Deshpande, Tushar and
Boehlen, Anne and Domingos, Cátia and Henning, Lukas and
Pitsch, Julika and Kim, Young-Bum and Bedner, Peter and
Steinhäuser, Christian and Henneberger, Christian},
title = {{E}pileptic activity triggers rapid {ROCK}1-dependent
astrocyte morphology changes.},
journal = {Glia},
volume = {72},
number = {3},
issn = {0894-1491},
address = {Bognor Regis [u.a.]},
publisher = {Wiley-Liss},
reportid = {DZNE-2024-00071},
pages = {643 - 659},
year = {2024},
abstract = {Long-term modifications of astrocyte function and
morphology are well known to occur in epilepsy. They are
implicated in the development and manifestation of the
disease, but the relevant mechanisms and their
pathophysiological role are not firmly established. For
instance, it is unclear how quickly the onset of epileptic
activity triggers astrocyte morphology changes and what the
relevant molecular signals are. We therefore used two-photon
excitation fluorescence microscopy to monitor astrocyte
morphology in parallel to the induction of epileptiform
activity. We uncovered astrocyte morphology changes within
10-20 min under various experimental conditions in acute
hippocampal slices. In vivo, induction of status epilepticus
resulted in similarly altered astrocyte morphology within 30
min. Further analysis in vitro revealed a persistent volume
reduction of peripheral astrocyte processes triggered by
induction of epileptiform activity. In addition, an impaired
diffusion within astrocytes and within the astrocyte network
was observed, which most likely is a direct consequence of
the astrocyte remodeling. These astrocyte morphology changes
were prevented by inhibition of the Rho GTPase RhoA and of
the Rho-associated kinase (ROCK). Selective deletion of
ROCK1 but not ROCK2 from astrocytes also prevented the
morphology change after induction of epileptiform activity
and reduced epileptiform activity. Together these
observations reveal that epileptic activity triggers a rapid
ROCK1-dependent astrocyte morphology change, which is
mechanistically linked to the strength of epileptiform
activity. This suggests that astrocytic ROCK1 signaling is a
maladaptive response of astrocytes to the onset of epileptic
activity.},
keywords = {Humans / Astrocytes / rho-Associated Kinases / Epilepsy /
Status Epilepticus / Hippocampus / ROCK signaling (Other) /
astrocytes (Other) / epilepsy (Other) / gap junction
coupling (Other) / morphology (Other) / remodeling (Other) /
rho-Associated Kinases (NLM Chemicals) / ROCK1 protein,
human (NLM Chemicals)},
cin = {AG Henneberger},
ddc = {610},
cid = {I:(DE-2719)1013029},
pnm = {351 - Brain Function (POF4-351)},
pid = {G:(DE-HGF)POF4-351},
typ = {PUB:(DE-HGF)16},
pmc = {pmc:PMC10842783},
pubmed = {pmid:38031824},
doi = {10.1002/glia.24495},
url = {https://pub.dzne.de/record/267062},
}