title: Development, plasticity and modulation of visceral afferents.
abstract: Visceral pain is the most common reason for doctor visits in the US. Like somatic pain, virtually all visceral pain sensations begin with the activation of primary sensory neurons innervating the viscera and/or the blood vessels associated with these structures. Visceral afferents also play a central role in tissue homeostasis. Recent studies show that in addition to monitoring the state of the viscera, they perform efferent functions through the release of small molecules (e.g. peptides like CGRP) that can drive inflammation, thereby contributing to the development of visceral pathologies (e.g. diabetes Razavi, R., Chan, Y., Afifiyan, F.N., Liu, X.J., Wan, X., Yantha, J., Tsui, H., Tang, L., Tsai, S., Santamaria, P., Driver, J.P., Serreze, D., Salter, M.W., Dosch, H.M., 2006. TRPV1+ sensory neurons control beta cell stress and islet inflammation in autoimmune diabetes, Cell 127 1123-1135). Visceral afferents are heterogeneous with respect to their anatomy, neurochemistry and function. They are also highly plastic in that their cellular environment continuously influences their response properties. This plasticity makes them susceptible to long-term changes that may contribute significantly to the development of persistent pain states such as those associated with irritable bowel syndrome, pancreatitis, and visceral cancers. This review examines recent insights into visceral afferent anatomy and neurochemistry and how neonatal insults can affect the function of these neurons in the adult. New approaches to the treatment of visceral pain, which focus on primary afferents, will also be discussed.
authors.affiliation: University of Pittsburgh School of Medicine, Pittsburgh Center for Pain Research, 200 Lothrop St., Pittsburgh, PA 16261, USA.
authors.forename: Julie A
authors.initials: JA
authors.lastname: Christianson
authors.forename: Klaus
authors.initials: K
authors.lastname: Bielefeldt
authors.forename: Christophe
authors.initials: C
authors.lastname: Altier
authors.forename: Nicolas
authors.initials: N
authors.lastname: Cenac
authors.forename: Brian M
authors.initials: BM
authors.lastname: Davis
authors.forename: Gerald F
authors.initials: GF
authors.lastname: Gebhart
authors.forename: Karin W
authors.initials: KW
authors.lastname: High
authors.forename: Marian
authors.initials: M
authors.lastname: Kollarik
authors.forename: Alan
authors.initials: A
authors.lastname: Randich
authors.forename: Brad
authors.initials: B
authors.lastname: Undem
authors.forename: Nathalie
authors.initials: N
authors.lastname: Vergnolle
mesh_terms: D000818:Animals; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology; D009479:Neuropeptides / Q000378:metabolism; D009619:Nociceptors / Q000378:metabolism*; D010146:Pain / Q000209:etiology / Q000503:physiopathology*; D011984:Sensory Receptor Cells / Q000378:metabolism*; D050916:TRPV Cation Channels / Q000378:metabolism; D014781:Viscera / Q000294:innervation* / Q000503:physiopathology; D017833:Visceral Afferents / Q000254:growth & development / Q000503:physiopathology*
chemical_list: D009479:Neuropeptides; D050916:TRPV Cation Channels; C494482:TRPV1 protein, human