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Abstract
NGF is a well-known neurotrophic factor essential for the survival and maintenance of primary afferent neurons and sympathetic neurons. NGF is also an inflammatory mediator associated with pain and itch. Congenital insensitivity to pain with anhidrosis is a genetic disorder due to loss-of-function mutations in the NTRK1 gene encoding TrkA, a receptor tyrosine kinase for NGF. Since patients with congenital insensitivity to pain with anhidrosis lack NGF-dependent unmyelinated (C-) and thinly myelinated (Aδ-) fibers, and their dermal sweat glands are without innervation, they exhibit no pain, itch, signs of neurogenic inflammation or sympathetic skin responses. Based on the pathophysiology of congenital insensitivity to pain with anhidrosis, this article indicates how NGF-dependent neurons are essential for the establishment of neural networks for interoception and homeostasis, and play crucial roles in brain–immune–endocrine interactions in pain, itch and inflammation. In addition, it refers to involvements of the NGF-TrkA system in various disease states, and potential pharmacological effects when this system is targeted.
Financial & competing interests disclosure
This work was supported in part by the Japan Society for the Promotion of Science (JSPS) (KAKENHI) Grant-in-Aid for Scientific Research (C) (21600010) and by the Ministry of Health, Labour and Welfare: Health and Labour Sciences Research Grants (Research on Intractable Diseases). The author has no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.