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Neural Plasticity
Volume 2016, Article ID 2769735, 11 pages
Review Article

Neuroplasticity and Repair in Rodent Neurotoxic Models of Spinal Motoneuron Disease

Department of Biomedical and Biotechnological Sciences, Physiology Section, University of Catania, Via Santa Sofia 64, 95125 Catania, Italy

Received 30 January 2015; Revised 12 July 2015; Accepted 19 August 2015

Academic Editor: Brandon A. Miller

Copyright © 2016 Rosario Gulino. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Retrogradely transported toxins are widely used to set up protocols for selective lesioning of the nervous system. These methods could be collectively named “molecular neurosurgery” because they are able to destroy specific types of neurons by using targeted neurotoxins. Lectins such as ricin, volkensin, or modeccin and neuropeptide- or antibody-conjugated saporin represent the most effective toxins used for neuronal lesioning. Some of these specific neurotoxins could be used to induce selective depletion of spinal motoneurons. In this review, we extensively describe two rodent models of motoneuron degeneration induced by volkensin or cholera toxin-B saporin. In particular, we focus on the possible experimental use of these models to mimic neurodegenerative diseases, to dissect the molecular mechanisms of neuroplastic changes underlying the spontaneous functional recovery after motoneuron death, and finally to test different strategies of neural repair. The potential clinical applications of these approaches are also discussed.