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  • Title: Sensitization to heat through G-protein-coupled receptor pathways in the isolated sciatic mouse nerve.
    Author: Fischer MJ, Reeh PW.
    Journal: Eur J Neurosci; 2007 Jun; 25(12):3570-5. PubMed ID: 17610576.
    Abstract:
    We have previously shown that isolated rat sciatic nerve axons express capsaicin, heat and proton sensitivity and respond to stimulation with a Ca(++)-dependent and graded calcitonin gene related peptide (CGRP) release. There is morphological evidence for stimulated vesicular exocytosis and for capsaicin receptor, transient receptor potential vanilloid type-1 (TRPV1, formerly VR1) translocation in the axolemma of unmyelinated nerve fibres. In sensory nerve terminals CGRP release in response to noxious heat can be sensitized by activation of G-protein-coupled receptors and related protein kinases. We present evidence that also in isolated mouse sciatic nerve axons the intracellular protein kinase A (PKA)- and C (PKC)-dependent transduction pathways modulate heat-induced (45 degrees C) CGRP release. This is demonstrated using the direct activators, forskolin and phorbol 12-myristate 13-acetate (PMA), as well as prostaglandin E2 (PGE(2)) and bradykinin acting through G-protein-coupled receptors. Inhibition at rest of protein kinases A or C left heat-induced CGRP release unchanged. In TRPV1 knockout animals no sensitization to heat was observed using a combined stimulation by prostaglandin E2 and bradykinin. To a surprising degree, peripheral nerve axons resemble peripheral sensory terminals in their common properties of sensory and signal transduction.
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