Primary sensory neurons have an inherent capacity for regeneration of their cut, crushed, or chemically lesioned axons. This capacity is displayed to a much greater extent after lesions of the peripheral axons than after lesions of their centrally directed axons. Additionally, the surrounding tissue determines to a significant extent the degree of recovery: whereas the peripheral nerve tissue provides neurotrophic support and a favorable environment for axonal growth, the central terminals of primary sensory neurons face a non-permissive and inhibitory glial tissue. Mechanical lesions of the peripheral axons of dorsal root ganglion (DRG) sensory neurons can be repaired by the intrinsic regenerative capacity of the neuron itself, when outgrowing axons from the proximal stump are able to transverse the tissue scar and reach the distal stump of the nerve. Bridging the gap with an autologous nerve graft or a short artificial graft filled with nerve growth factor (NGF) can improve recovery. Neurotoxic lesions of the axon terminals are effectively recovered by intermittent local or systemic NGF injections. A recovery from a diabetic sensory neuropathy probably requires the continuous delivery of NGF or additional neurotrophic factors. A recovery from a dorsal rhizotomy or from a dorsal column lesion can possibly be achieved by the concomitant transgene-mediated overexpression of neurotrophins, the transformation of the DRG neuron cells to a competence for regrowth, and the counteraction of the growth-inhibitory nature of the central nervous system tissue.

Keywords:
Nerve injury, Primary afferent neuron, Sensory neuropathy, Neurotoxin, Neuroregeneration, Nerve growth factor
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© 2003 S. Karger AG, Basel
2003
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