Antiepileptic effects of botulinum neurotoxin E

Laura Costantin, Yuri Bozzi, Cristina Richichi, Alessandro Viegi, Flavia Antonucci, Marcella Funicello, Marco Gobbi, Tiziana Mennini, Ornella Rossetto, Cesare Montecucco, Lamberto Maffei, Annamaria Vezzani, Matteo Caleo

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)1943-1951
Number of pages9
JournalJournal of Neuroscience
Issue number8
Publication statusPublished - Feb 23 2005


  • Hippocampal kindling
  • Kainic acid
  • Morris water maze
  • Neuronal death
  • Neurotransmitter release
  • Seizures

ASJC Scopus subject areas

  • Neuroscience(all)


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