Clinical and experimental studies clearly demonstrate that prolonged seizures and status epilepticus induce neuronal cell death in the brain. Recent evidence suggests that induction of apoptosis contributes greatly to seizure-induced brain damage. We recently demonstrated that intrahippocampal delivery of botulinum neurotoxin E (BoNT/E) in the rat hippocampus is able to prevent neuronal loss, which occurs after kainic-acid-induced seizures. Here, we investigated the molecular mechanisms of BoNT/E-mediated neuroprotection. We found that intrahippocampal administration of BoNT/E prevents the upregulation of apoptotic proteins (phosphorylated c-Jun and cleaved caspase 3), which occurs in hippocampal neurones following kainic acid seizures. These results demonstrate that the neuroprotective action of BoNT/E on seizure-injured hippocampal neurons involves the blockade of well-characterized apoptotic pathways.
BoNT/E prevents seizure-induced activation of caspase 3 in the rat hippocampus / I. Manno, F. Antonucci, M. Caleo, Y. Bozzi. - In: NEUROREPORT. - ISSN 0959-4965. - 18:6(2007), pp. 577-580.
|Titolo:||BoNT/E prevents seizure-induced activation of caspase 3 in the rat hippocampus|
|Parole Chiave:||apoptosis; botulinum neurotoxin; caspase; epilepsy; excitotoxicity; kainic acid; neuronal cell death; phosphorylated jun; programmed cell death|
|Settore Scientifico Disciplinare:||Settore BIO/14 - Farmacologia|
|Data di pubblicazione:||2007|
|Digital Object Identifier (DOI):||http://dx.doi.org/10.1097/WNR.0b013e32801b3cbb|
|Appare nelle tipologie:||01 - Articolo su periodico|