Animal models for studying motor axon terminal paralysis and recovery.
An extraordinary property of the peripheral nervous system is that nerve terminals can regenerate after damage caused by different physical, chemical, or biological pathogens. Regeneration is the result of a complex and ill-known interplay among the nerve, the glia, the muscle, the basal lamina and, in some cases, the immune system. This phenomenon has been studied using different injury models mainly in rodents, particularly in mice, where a lesion can be produced in a chosen anatomical area. These approaches differ significantly among them for the nature of the lesion and the final outcomes. We have reviewed here the most common experimental models employed to induce motor axon injury, the relative advantages and drawbacks, and the principal read-outs used to monitor the regenerative process. Recently introduced tools for inducing reversible damage to the motor axon terminal that overcome some of the drawbacks of the more classical approaches are also discussed. Animal models have provided precious information about the cellular components involved in the regenerative process and on its electrophysiological features. Methods and tools made available recently allow one to identify and study molecules that are involved in the crosstalk among the components of the endplate. The time-course of the intercellular signaling and of the intracellular pathways activated will draw a picture of the entire process of regeneration as seen from a privileged anatomical site of observation. This is an article for the special issue XVth International Symposium on Cholinergic Mechanisms.
Department of Biomedical Sciences, University of Padua, Padua, Italy.
Michela
0000-0003-1763-2648
M
Rigoni
Department of Biomedical Sciences, University of Padua, Padua, Italy.|CNR Institute of Neuroscience, Padua, Italy.
Cesare
C
Montecucco
D000818:Animals; D001369:Axons / Q000378:metabolism*; D006801:Humans; D009132:Muscles / Q000502:physiology*; D009416:Nerve Regeneration / Q000502:physiology*; D009457:Neuroglia / Q000502:physiology; D009469:Neuromuscular Junction / Q000378:metabolism*; D017729:Presynaptic Terminals / Q000502:physiology*
Schwann cells; motor axon regeneration; neuromuscular junction; neurotoxins; peripheral nerve injury