Epilepsy-induced abnormal striatal plasticity in Bassoon mutant mice

Veronica Ghiglieri, Barbara Picconi, Carmelo Sgobio, Vincenza Bagetta, Ilaria Barone, Vincent Paillè, Massimiliano Di Filippo, Federica Polli, Fabrizio Gardoni, Wilko Altrock, Eckart D. Gundelfinger, Giovambattista De Sarro, Giorgio Bernardi, Martine Ammassari-Teule, Monica Di Luca, Paolo Calabresi

Research output: Contribution to journalArticlepeer-review


Recently, the striatum has been implicated in the spread of epileptic seizures. As the absence of functional scaffolding protein Bassoon in mutant mice is associated with the development of pronounced spontaneous seizures, we utilized this new genetic model of epilepsy to investigate seizure-induced changes in striatal synaptic plasticity. Mutant mice showed reduced long-term potentiation in striatal spiny neurons, associated with an altered N-methyl-d-aspartate (NMDA) receptor subunit distribution, whereas GABAergic fast-spiking (FS) interneurons showed NMDA-dependent short-term potentiation that was absent in wild-type animals. Alterations in the dendritic morphology of spiny neurons and in the number of FS interneurons were also observed. Early antiepileptic treatment with valproic acid reduced epileptic attacks and mortality, rescuing physiological striatal synaptic plasticity and NMDA receptor subunit composition. However, morphological alterations were not affected by antiepileptic treatment. Our results indicate that, in Bsn mutant mice, initial morphological alterations seem to reflect a more direct effect of the abnormal genotype, whereas plasticity changes are likely to be caused by the occurrence of repeated cortical seizures.

Original languageEnglish
Pages (from-to)1979-1993
Number of pages15
JournalEuropean Journal of Neuroscience
Issue number10
Publication statusPublished - May 2009


  • Dorsolateral striatum
  • Fast-spiking interneurons
  • Postsynaptic density
  • Scaffolding proteins
  • Synaptic plasticity

ASJC Scopus subject areas

  • Neuroscience(all)


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