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Epilepsy‐induced abnormal striatal plasticity in Bassoon mutant mice
Author(s) -
Ghiglieri Veronica,
Picconi Barbara,
Sgobio Carmelo,
Bagetta Vincenza,
Barone Ilaria,
Paillè Vincent,
Di Filippo Massimiliano,
Polli Federica,
Gardoni Fabrizio,
Altrock Wilko,
Gundelfinger Eckart D.,
De Sarro Giovambattista,
Bernardi Giorgio,
AmmassariTeule Martine,
Di Luca Monica,
Calabresi Paolo
Publication year - 2009
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2009.06733.x
Subject(s) - medium spiny neuron , nmda receptor , long term potentiation , neuroscience , striatum , synaptic plasticity , gabaergic , biology , glutamate receptor , dendritic spine , neuroplasticity , epilepsy , receptor , inhibitory postsynaptic potential , genetics , dopamine , hippocampal formation
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.