Journal
EUROPEAN JOURNAL OF NEUROSCIENCE
Volume 27, Issue 7, Pages 1700-1709Publisher
WILEY
DOI: 10.1111/j.1460-9568.2008.06131.x
Keywords
estrogen; intracellular signalling; nociception; pain
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We evaluated the signalling pathway by which estrogen acts in peripheral tissue to produce protein kinase C epsilon (PKC epsilon)-dependent mechanical hyperalgesia. Specific agonists for the classical estrogen receptors (ER), ER alpha and ER beta, did not result in activation of PKC epsilon in neurons of dissociated rat dorsal root ganglia. In contrast, G-1, a specific agonist of the recently identified G-protein-coupled estrogen receptor, GPR30, induced PKC epsilon translocation. Involvement of GPR30 and independence of ER alpha and ER beta was confirmed using the GPR30 agonist and simultaneous ER alpha and ER beta antagonist ICI 182,780 (fulvestrant). The GPR30 transcript could be amplified from dorsal root ganglia tissue. We found estrogen-induced as well as GPR30-agonist-induced PKC epsilon translocation to be restricted to the subgroup of nociceptive neurons positive for isolectin IB4 from Bandeiraea simplicifolia. Corroborating the cellular results, both GPR30 agonists, G-1 as well as ICI 182,780, resulted in the onset of PKC epsilon-dependent mechanical hyperalgesia if injected into paws of adult rats. We therefore suggest that estrogen acts acutely at GPR30 in nociceptors to produce mechanical hyperalgesia.
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