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Neural Plasticity
Volume 2017 (2017), Article ID 2652560, 7 pages
Research Article

Pilocarpine-Induced Status Epilepticus Is Associated with Changes in the Actin-Modulating Protein Synaptopodin and Alterations in Long-Term Potentiation in the Mouse Hippocampus

1Department of Neurology, The Chaim Sheba Medical Center, Tel HaShomer, Israel
2Institute of Anatomy II, Faculty of Medicine, Heinrich-Heine University, Düsseldorf, Germany
3Institute of Clinical Neuroanatomy, Neuroscience Center Frankfurt, Goethe University, Frankfurt, Germany
4Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
5Talpiot Medical Leadership Program, The Chaim Sheba Medical Center, Tel HaShomer, Israel
6Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
7Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel

Correspondence should be addressed to Andreas Vlachos and Nicola Maggio

Received 1 August 2016; Revised 12 October 2016; Accepted 13 October 2016; Published 5 January 2017

Academic Editor: Alvaro O. Ardiles

Copyright © 2017 Maximilian Lenz et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Epilepsy is a complex neurological disorder which can severely affect neuronal function. Some patients may experience status epilepticus, a life-threatening state of ongoing seizure activity associated with postictal cognitive dysfunction. However, the molecular mechanisms by which status epilepticus influences brain function beyond seizure activity remain not well understood. Here, we addressed the question of whether pilocarpine-induced status epilepticus affects synaptopodin (SP), an actin-binding protein, which regulates the ability of neurons to express synaptic plasticity. This makes SP an interesting marker for epilepsy-associated alterations in synaptic function. Indeed, single dose intraperitoneal pilocarpine injection (250 mg/kg) in three-month-old male C57BL/6J mice leads to a rapid reduction in hippocampal SP-cluster sizes and numbers (in CA1 stratum radiatum of the dorsal hippocampus; 90 min after injection). In line with this observation (and previous work using SP-deficient mice), a defect in the ability to induce long-term potentiation (LTP) of Schaffer collateral-CA1 synapses is observed. Based on these findings we propose that status epilepticus could exert its aftereffects on cognition at least in part by perturbing SP-dependent mechanisms of synaptic plasticity.