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@ARTICLE{Kherbouche:281346,
author = {Kherbouche, Oussama and Henning, Lukas and Niemann, Pia and
Geisen, Caroline and Seifert, Gerald and Henneberger,
Christian and Fleischmann, Bernd K and Steinhäuser,
Christian and Bedner, Peter},
title = {{I}nduced {O}verexpression of {C}onnexin43 in {A}strocytes
{A}ttenuates the {P}rogression of {E}xperimental {T}emporal
{L}obe {E}pilepsy.},
journal = {Neurochemical research},
volume = {50},
number = {5},
issn = {0364-3190},
address = {Dordrecht [u.a.]},
publisher = {Springer Science + Business Media B.V},
reportid = {DZNE-2025-01093},
pages = {303},
year = {2025},
abstract = {Astrocytic gap junctional communication plays a critical
role in regulating neuronal activity and network
synchronization, yet its precise contributions to brain
function and the pathogenesis of neurological disorders
remains incompletely understood. To address this, we
generated a transgenic mouse line with inducible,
astrocyte-specific overexpression of the gap junction
protein connexin43 (Cx43). In these mice, hippocampal
astrocytes exhibited markedly elevated Cx43 protein levels
and a ~ $20\%$ increase in intercellular gap junction
coupling. Enhanced coupling was accompanied by a reduction
in astrocytic cell volume and branching, without affecting
passive membrane properties or astrocyte density in the
hippocampus. Cx43 overexpression had no detectable impact on
adult neurogenesis in the dentate gyrus, nor did it alter
hippocampal synaptic efficacy or plasticity. Notably, in a
mouse model of temporal lobe epilepsy with hippocampal
sclerosis, astrocytic Cx43 overexpression attenuated chronic
epileptic activity and the extent of sclerosis, supporting
an antiepileptic role of the astroglial network.
Collectively, these findings enhance our understanding of
the functional relevance of astrocytic gap junction coupling
in health and disease, with potential implications for the
design of new treatment strategies.},
keywords = {Animals / Astrocytes: metabolism / Connexin 43:
biosynthesis / Connexin 43: genetics / Epilepsy, Temporal
Lobe: metabolism / Epilepsy, Temporal Lobe: pathology /
Mice, Transgenic / Mice / Disease Progression / Hippocampus:
metabolism / Hippocampus: pathology / Mice, Inbred C57BL /
Gap Junctions: metabolism / Male / Connexin 43 (Other) / EEG
(Other) / Electrophysiology (Other) / Gap junction coupling
(Other) / Hippocampal sclerosis (Other) / Temporal lobe
epilepsy (Other) / Connexin 43 (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},
pubmed = {pmid:40965686},
pmc = {pmc:PMC12446404},
doi = {10.1007/s11064-025-04558-w},
url = {https://pub.dzne.de/record/281346},
}