Botulinum neurotoxin E (BoNT/E) reduces CA1 neuron loss and granule cell dispersion, with no effects on chronic seizures, in a mouse model of temporal lobe epilepsy

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• 作者：Flavia Antonucci ; Angelo Di Garbo ; Elena Novelli ; Ilaria Manno ; Ferdin ; o Sartucci ; Yuri Bozzi ; Matteo Caleo
• 关键词：Kainic acid ; Hippocampus ; Neurotransmitter release ; Spontaneous recurrent seizures ; Epileptogenesis ; Latent period
• 刊名：Experimental Neurology
• 出版年：2008
• 出版时间：April 2008
• 年：2008
• 卷：210
• 期：2
• 页码：388-401
• 全文大小：1468 K

文摘

Mesial temporal lobe epilepsy (MTLE) is often the result of an early insult that induces a reorganization in hippocampal circuitry leading, after a latent period, to chronic epilepsy. Hippocampal rearrangements during the latent phase include neuronal loss, axonal and dendritic plasticity, neurogenesis, and cell repositioning, but the role of these changes in epilepsy development is unclear. Here we have tested whether administration of the synaptic blocker botulinum neurotoxin E (BoNT/E) interferes with development of spontaneous seizures and histopathological changes following an episode of status epilepticus (SE). SE was induced by unilateral intrahippocampal injection of kainic acid in mice and BoNT/E was delivered to the same hippocampus 3 h later. We found that treatment with BoNT/E prolonged the duration of the latent period but did not block the occurrence of spontaneous seizures. At the histopathological level, BoNT/E reduced loss of CA1 pyramidal neurons and dispersion of dentate granule cells. Downregulation of reelin expression along the hippocampal fissure was also suppressed by BoNT/E treatment.