Abstract
Sensory C-fibres are assumed to have a dual function in response to injury. Besides their central activity, they appear to contribute to inflammatory reactions in the periphery (1–3). Antidromic electrical stimulation as well as stimulation by chemical irritants or noxious heat lead to vasodilatation and plasma protein extravasation (4–6). These responses, which are also called “neurogenic inflammation” (see 7,8) are assumed to be caused by a mediator released from peripheral endings of C-fibres. Many of the criteria for being the mediator of these effects are fulfilled by substance P (SP) (9). However, two SP-related peptides have recently been isolated from mammalian spinal cord, i.e. neurokinin A (NKA) (10–12) and neurokinin B (NKB) (10,13). A common precursor gene for SP and NKA has been identified in the CNS (11), the mRNA of which is also present in sensory neurones (14). Thus, it can be assumed that SP coexists with NKA. Additionally, SP seems to coexist with calcitonin gene-related peptide (CGRP) in cells of spinal ganglia (15) and a release of CGRP from sensory neurones in culture has been demonstrated (16).
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Saria, A., Lundberg, J.M. (1985). Neurogenic Inflammation. In: Higgs, G.A., Williams, T.J. (eds) Inflammatory Mediators. Satellite Symposia of the IUPHAR 9th International Congress of Pharmacology. Palgrave Macmillan, London. https://doi.org/10.1007/978-1-349-07834-9_8
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