Abstract |
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.
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Authors | Ilaria Manno, Flavia Antonucci, Matteo Caleo, Yuri Bozzi |
Journal | Neuroreport
(Neuroreport)
Vol. 18
Issue 6
Pg. 577-80
(Apr 16 2007)
ISSN: 0959-4965 [Print] England |
PMID | 17413660
(Publication Type: Duplicate Publication, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Excitatory Amino Acid Agonists
- Neuroprotective Agents
- Casp3 protein, rat
- Caspase 3
- Botulinum Toxins
- Kainic Acid
- botulinum toxin type E
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Topics |
- Animals
- Apoptosis
(drug effects)
- Botulinum Toxins
(pharmacology)
- Caspase 3
(metabolism)
- Disease Models, Animal
- Drug Interactions
- Enzyme Activation
(drug effects)
- Excitatory Amino Acid Agonists
- Hippocampus
(drug effects, pathology)
- Kainic Acid
- Male
- Neurons
(drug effects)
- Neuroprotective Agents
(pharmacology)
- Rats
- Rats, Sprague-Dawley
- Seizures
(chemically induced, pathology)
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