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Nerve Growth Factor and Neuropathic Pain

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Pathogenesis of Neuropathic Pain
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Abstract

Nerve growth factor is probably the best studied of all the neurotrophins or neuronal growth factors. These all bind with varying degrees of specifically to NT receptors. The expression of NGF afternoon acute insult and subsequent hyperexcitability is a common pathway that we likely observe in the development of neuropathic pain syndromes. NGF signaling is mediated via binding at the p75NTR and TrkA receptor with the TrkA receptor exhibiting picomolar affinity and selectivity to NGF in the presence of other neurotrophins. NGF binding at the p75NTR receptor may result in either apoptosis or cell survival pathways. The binding of NGF to TrkA is thought to be responsible for neuronal survival and neuronal differentiation. When NGF is dysregulated neuropathic pain results and augmented neurite outgrowth with concomitant nociceptor sensitivity occurs. NGF plays critical roles in mediation of inflammation, the development of neuropathy, CNS-mediated analgesia in diabetic neuropathy, the development and maintenance of sensory neurons, the promotion of sensory and sympathetic neuronal survival; and the mediation of pain. Molecular as well as genetic interventions have been developed which target the interaction of NGF and the TrkA receptor. This chapter focuses upon these roles in a number of neuropathic syndromes and therapeutic approaches to neuropathic pain mediated by NGF.

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Malomo, A., Smith, D.I. (2022). Nerve Growth Factor and Neuropathic Pain. In: Smith, D.I., Tran, H. (eds) Pathogenesis of Neuropathic Pain. Springer, Cham. https://doi.org/10.1007/978-3-030-91455-4_1

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