| Autor: |
Costantin, Laura, Bozzi, Yuri, Richichi, Cristina, Viegi, Alessandro, Antonucci, Flavia, Funicello, Marcella, Gobbi, Marco, Mennini, Tiziana, Rossetto, Ornella, Montecucco, Cesare, Maffei, Lamberto, Vezzani, Annamaria, Caleo, Matteo |
| Předmět: |
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| Zdroj: |
Journal of Neuroscience; 2/23/2005, Vol. 25 Issue 8, p1943-1951, 9p, 3 Diagrams, 6 Graphs |
| Abstrakt: |
Experimental studies suggest that the delivery of antiepileptic agents into the seizure focus might be of potential utility for the treatment of focal-onset epilepsies. Botulinum neurotoxin E (BoNT/E) causes a prolonged inhibition of neurotransmitter release after its specific cleavage of the synaptic protein synaptosomal-associated protein of 25 kDa (SNAP-25). Here, we show that BoNT/E injected into the rat hippocampus inhibits glutamate release and blocks spike activity of pyramidal neurons. BoNT/E effects persist for at least 3 weeks, as determined by immunodetection of cleaved SNAP-25 and loss of intact SNAP-25. The delivery of BoNT/E to the rat hippocampus dramatically reduces both focal and generalized kainic acid-induced seizures as documented by behavioral and electrographic analysis. BoNT/E treatment also prevents neuronal loss and long-term cognitive deficits associated with kainic acid seizures. Moreover, BoNT/E-injected rats require 50% more electrical stimulations to reach stage 5 of kindling, thus indicating a delayed epileptogenesis. We conclude that BoNT/E delivery to the hippocampus is both antiictal and antiepileptogenic in experimental models of epilepsy. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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