Pilocarpine mimics temporal lobeepilepsy by inducing SE associatedwith damage in hippocampal andextrahippocampal areas. We havecharacterized a vascular lesion thatdestroys the perforant path (PP) inCA3 after SE. This lesion (white arrows,Figure 1) was evident withmagnetic resonance imaging 1 day aftera SE lasting for 120 min and its appearancewas delayed by limiting SEto 60 or 30 min. Rats exposed to SEfor 30 min developed the lesion unlesssubsequently treated with diazepam(20 mg/kg s.c. for 3 days), whichprotected 50% of the animals. Antibodiesfor astrocytes (GFAP), dendrites(MAP2) and PPnerve terminals(mGluR2/3), showed areas of immunoreactivityloss in which we localizedincreased staining for laminin, inthe basement membrane of vessels.This lesion was uncommon in young(3-week-old) rats. The latent periodfor seizure appearance was similar inadult rats exposed to SE only or to SEfollowed by neuroprotection with diazepam;however, the frequency ofspontaneous seizures was significantlylower (p < 0.01) in the neuroprotectedgroup. Moreover, spontaneousseizures were delayed in youngrats (p < 0.01) exposed to 60 min SEcompared to adults experiencing asimilar SE. To investigate the role ofdamaged CA3 in seizure activity, were-induced SE in adult and young epilepticrats. Using FosB/FosB markers,we found induction of FosB/FosB immunopositivity in CA3neurons of young but not in adult rats.These experiments reveal that SE canproduce a focal lesion in the PP, whichaffects the role of the hippocampus inepileptic rats.
|Data di pubblicazione:||2008|
|Titolo:||Characterizationof a focal vascular lesionaffecting entorhinalcortex-CA3connections after statusepilepticus|
|Autori:||G. Biagini; D. Longo; E. Baldelli;M. Contri; P. Nichelli; U.Guerrini; L. Sironi; P. Gelosa;G. Bertazzoni; M. Avoli|
|Nome del convegno:||9th European Congress of Neuropathology|
|Luogo del convegno:||Athens, Greece|
|Data del convegno:||8-10/05/2008|
|Titolo del libro:||Volume 27|
|Appare nelle tipologie:||Abstract in Rivista|
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