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Activity‐dependent phosphorylation of Akt/PKB in adult DRG neurons
Author(s) -
Pezet Sophie,
Spyropoulos Achillefs,
Williams Robert J.,
McMahon Stephen B.
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2005.04011.x
Subject(s) - protein kinase b , phosphorylation , pi3k/akt/mtor pathway , dorsal root ganglion , nociceptor , microbiology and biotechnology , chemistry , signal transduction , biology , neuroscience , nociception , receptor , sensory system , biochemistry
The serine/threonine kinase Akt/PKB has been implicated in cell survival signalling in many cell types, including the dorsal root ganglion (DRG). However, little is known about its role in physiological and pathophysiological conditions in the adult sensory and nociceptive system. In this study, we show that in naïve animals almost all cells express Akt but only a subset of small‐diameter neurons expresses a high level of phospho‐Akt (p‐Akt Ser 473). Activation of peripheral nociceptors in vivo using intraplantar injections of capsaicin in anaesthetized rats induced a rapid onset and time‐dependent increase in p‐Akt Ser 473 in small‐ and medium‐sized DRG, predominantly TRPV1‐positive neurons. In addition, electrical stimulation of ‘A and C’ fibres in the sciatic nerve induced an increase in the cytoplasmic staining of p‐Akt Ser 473 in small‐ and medium‐size DRG neurons. Blocking neuronal activity in the sciatic nerve using tetrodotoxin reduced the basal level of p‐Akt Ser 473. Cultured DRG neurons confirmed that phosphorylation of Akt in different cellular compartments is triggered by depolarization or receptor activation, and suggested that this effect is mediated in part by phosphatidylinositol 3‐kinase. Our results show that p‐Akt Ser 473 is a marker of nociceptor activation and suggest a novel role for Akt in the transduction of intracellular signals in adult DRG neurons.