Open AccessProtein kinase C modulation of thermo-sensitive transient receptor potential channels: Implications for pain signaling
Author(s) -
Sravan Mandadi,
Patricia J. Armati,
Basil D. Roufogalis
Publication year - 2011
Publication title -
journal of natural science, biology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.236
H-Index - 30
eISSN - 2229-7707
pISSN - 0976-9668
DOI - 10.4103/0976-9668.82311
Subject(s) - transient receptor potential channel , trpv1 , protein kinase c , dorsal root ganglion , trpm8 , chronic pain , neuroscience , gene isoform , nociception , medicine , signal transduction , receptor , microbiology and biotechnology , sensory system , chemistry , biology , biochemistry , gene
A variety of molecules are reported to be involved in chronic pain. This review outlines the specifics of protein kinase C (PKC), its isoforms and their role in modulating thermo-sensitive transient receptor potential (TRP) channels TRPV1-4, TRPM8, and TRPA1. Anatomically, PKC and thermo-sensitive TRPs are co-expressed in cell bodies of nociceptive dorsal root ganglion (DRG) neurons, which are used as physiological correlates of peripheral and central projections involved in pain transmission. In the past decade, modulation of painful heat-sensitive TRPV1 by PKC has received the most attention. Recently, PKC modulation of other newly discovered thermo-sensitive pain-mediating TRPs has come into focus. Such modulation may occur under conditions of chronic pain resulting from nerve damage or inflammation. Since thermo-TRPs are primary detectors of acute pain stimuli, their modulation by PKC can severely alter their function, resulting in chronic pain. Comprehensive knowledge of pain signaling involving interaction of specific isoforms of PKC with specific thermo-sensitive TRP channels is incomplete. Such information is necessary to dissect out modality specific mechanisms to better manage the complex polymodal nature of chronic pain. This review is an attempt to update the readers on current knowledge of PKC modulation of thermo-sensitive TRPs and highlight implications of such modulation for pain signaling.