Cited by 159Epilepsy research and treatmentNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms

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Kainate Seizures Cause Acute Dendritic Injury and Actin Depolymerization In Vivo

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Zeng, Ling-Hui, Xu, Lin, Rensing, Nicholas R., Sinatra, Philip M., Rothman, Steven M., Wong, Michael·2007·The Journal of Neuroscience

DOI 10.1523/jneurosci.0983-07.2007PMC PMC3934634

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Abstract

Seizures may cause brain injury via a variety of mechanisms, potentially contributing to cognitive deficits in epilepsy patients. Although seizures induce neuronal death in some situations, they may also have “nonlethal” pathophysiological effects on neuronal structure and function, such as modifying dendritic morphology. Previous studies involving conventional fixed tissue analysis have demonstrated a chronic loss of dendritic spines after seizures in animal models and human tissue. More recently,in vivo time-lapse imaging methods have been used to monitor acute changes in spines directly during seizures, but documented spine loss only under severe conditions. Here, we examined effects of secondary generalized seizures induced by kainate, on dendritic structure of neocortical neurons using multiphoton imaging in live mice in vivo and investigated molecular mechanisms mediating these structural changes. Higher-stage kainate-induced seizures caused dramatic dendritic beading and loss of spines within minutes, in the absence of neuronal death or changes in systemic oxygenation. Although the dendritic beading improved rapidly after the seizures, the spine loss recovered only partially over a 24 h period. Kainate seizures also resulted in activation of the actin-depolymerizing factor, cofilin, and a corresponding decrease in filamentous actin, indicating that depolymerization of actin may mediate the morphological dendritic changes. Finally, an inhibitor of the calcium-dependent phosphatase, calcineurin, antagonized the effects of seizures on cofilin activation and spine morphology. These dramatic in vivo findings demonstrate that seizures produce acute dendritic injury in neocortical neurons via calcineurin-dependent regulation of the actin cytoskeleton, suggesting novel therapeutic targets for preventing seizure-induced brain injury.

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Authors: Zeng, L.-H., Xu, L., Rensing, N. R., Sinatra, P. M., Rothman, S. M., & Wong, M.
Affiliations: Washington University in St. Louis (US)
ORCID: Xu, Lin
Wong, Michael
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2007-10-24
Volume: 27
Issue: 43
Pages: 11604-11613
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.0983-07.2007
PMC: PMC3934634
OpenAlex: W2081333064
Cited by: 158
References: 44
Citations by year: 2026: 3 · 2025: 1 · 2024: 8 · 2023: 12 · 2022: 6 · 2021: 7 · 2020: 9 · 2019: 8 · 2018: 2 · 2017: 8 · 2016: 13 · 2015: 11 · 2014: 9 · 2013: 10 · 2012: 9
FWCI: 6.46
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 183 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
Funders: National Institutes of Health (NS057105)
National Institute of Neurological Disorders and Stroke (R01 NS42936, P30NS057105, NS057105, K02NS045583, R21NS045652, R01NS042936, R01NS056872)
Topics: Health Sciences › Medicine › Clinical Neurology › Epilepsy research and treatment
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords: kainate-induced seizures, secondary generalized seizures, dendritic spines, actin depolymerization, cofilin, calcineurin, actin cytoskeleton, neocortical neurons, seizure-induced brain injury, dendritic morphology, epilepsy
MeSH terms: Actins, Animals, Cytoskeleton, Dendrites, Kainic Acid, Mice, Inbred C57BL, Mice, Transgenic, Seizures, Dendritic Spines, Destrin, Mice

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Kainate Seizures Cause Acute Dendritic Injury and Actin Depolymerization In Vivo

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