Kainate-induced epileptic seizures induce a recruitment of caldendrin to the postsynaptic density in rat brain.

Karl Heinz Smalla, Constanze I. Seidenbecher, Wolfgang Tischmeyer, Horst Schicknick, Ursula Wyneken, Tobias M. Böckers, Eckart D. Gundelfinger, Michael R. Kreutz*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Caldendrin defines a novel family of neuronal calcium-sensor proteins, the C-terminal moiety of which displays high similarity to calmodulin. We now report that the protein is recruited to the postsynaptic density (PSD) of cortical and hippocampal neurons in response to kainate-induced epileptic seizures, an animal model of human temporal lobe epilepsy. The translocation of caldendrin to the PSD did not occur in kainate-treated rats that did not develop seizures. The enhanced PSD levels of caldendrin are not due to increased protein synthesis and most likely reflect a recruitment from the soluble caldendrin protein pool. These findings suggest that the transduction of dendritic Ca2+-signals via caldendrin is altered by epileptic seizures and that caldendrin might be involved in the pathophysiology of temporal lobe epilepsy.

Original languageEnglish
Pages (from-to)159-162
Number of pages4
JournalMolecular Brain Research
Issue number1-2
StatePublished - 19 Aug 2003

Bibliographical note

Funding Information:
The authors gratefully acknowledge the professional technical assistance of C. Borutzki and M. Marunde. Supported by the DFG (Kr1879/2-1, 2-2), the Volkswagen Foundation, the Fonds der Chemischen Industrie and the Land Sachsen-Anhalt (FKZ: 2508A/0086; 3004A/0088H).


  • Cytoskeleton
  • EF-hand protein
  • Seizures
  • Synapse
  • Temporal lobe epilepsy


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