RESEARCH ARTICLE
Contribution of Ion Channel Trafficking to Nociceptor Sensitization
M. Camprubí-Robles1, 3, A. Ferrer-Montiel1, R. Planells-Cases*, 2
Article Information
Identifiers and Pagination:
Year: 2010Volume: 3
First Page: 108
Last Page: 116
Publisher ID: TOPAINJ-3-108
DOI: 10.2174/1876386301003010108
Article History:
Received Date: 10/09/2009Revision Received Date: 20/09/2009
Acceptance Date: 18/08/2010
Electronic publication date: 28/9/2010
Collection year: 2010
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Nociceptor sensitization is a process triggered by proinflammatory factors that result in a significant increase in neuronal excitability by affecting both the threshold and frequency of action potential firing. The increased sensory neuron activity is due to a metabolic change produced by the activation of intracellular signaling cascades that usually alter the expression and functionality of molecular sensors present in the neuronal surface, i.e. ion channels and metabotropic receptors. Cumulative evidence is showing that inflammatory sensitization of nociceptors is significantly contributed by an enhanced expression of ion channels that directly influence neuronal excitability. Furthermore, recent data indicates that mobilization and regulated exocytosis of a ready-to-go vesicular population of channels as a pivotal event underlying acute inflammatory sensitization of sensory neurons; whereas an increment in transcription and/or translation and trafficking is involved in chronic neuronal sensitization. Therefore, identification of the molecular components involved in channel trafficking and exocytosis in the inflamed terminal may provide new strategies for attenuating nociceptor sensitization and their consequences, namely hyperalgesia and allodynia.
