title: Neuroplasticity and Repair in Rodent Neurotoxic Models of Spinal Motoneuron Disease.
abstract: 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.
authors: Department of Biomedical and Biotechnological Sciences, Physiology Section, University of Catania, Via Santa Sofia 64, 95125 Catania, Italy.
authors: Rosario
authors: R
authors: Gulino
mesh_terms: D000818:Animals; D002772:Cholera Toxin; D004195:Disease Models, Animal; D009410:Nerve Degeneration / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D009416:Nerve Regeneration / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D051381:Rats; D054789:Ribosome Inactivating Proteins, Type 1; D054790:Ribosome Inactivating Proteins, Type 2; D000076985:Saporins
chemical_list: D054789:Ribosome Inactivating Proteins, Type 1; D054790:Ribosome Inactivating Proteins, Type 2; C420112:cholera toxin B-saporin conjugate; D002772:Cholera Toxin; C049134:volkensin; D000076985:Saporins