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Matteo Caleo

       

Botulinum neurotoxins,

 

The main topic of our group is the study of the effects of botulinum neurotoxins (BoNTs) in the brain. BoNTs (seven serotypes, indicated A-G) are bacterial enzymes that block transmitter release via the cleavage of specific components of the vesicle fusion machinery. We recently found that BoNT/A exhibits retrograde axonal transport following uptake at the nerve terminal. This finding has implications for the clinical uses of BoNT/A.

Our work demonstrates that BoNTs are powerful tools to block neuronal communication in the brain for varying durations. We are exploiting the silencing properties of BoNTs in different experimental studies.

First, we are employing BoNTs to address the role of neural activity during visual system development and plasticity. In a recent study, we have shown that a BoNT/E-mediated, transient unilateral silencing of rat striate cortex during postnatal development has lasting effects on visual function and plasticity. Indeed, visual abilities are permanently reduced in the blocked hemisphere, and the critical period for ocular dominance plasticity persists into adulthood. Remarkably, these effects extend equally to the contralateral uninjected side, revealing a role for interhemispheric connections in cortical development.

Second, we have been evaluating the anticonvulsant and antiepileptogenic properties of BoNT/E in rodent models of temporal lobe epilepsy. Specifically, we have shown that BoNT/E application to the hippocampus has anticonvulsant and neuroprotective effects in rodent models of temporal lobe seizures.

 

 

visual system plasticity,

epilepsy

 

 

F. Antonucci et al. (2008)

Long-distance retrograde effects of botulinum neurotoxin A. 

J. Neurosci. 28: 3689-3696.

   
M. Caleo et al. (2007)

Transient synaptic silencing of developing striate cortex has persistent effects on visual function and plasticity.

J. Neurosci. 27: 4530-40.
   
L. Costantin et al. (2005)
Antiepileptic effects of botulinum neurotoxin E (BoNT/E).
J. Neurosci. 25: 1943-1951.