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Sex hormones regulate the contribution of PKCε and PKA signalling in inflammatory pain in the rat
Author(s) -
Dina Olayinka A.,
Aley K. O.,
Isenberg William,
Messing Robert O.,
Levine Jon D.
Publication year - 2001
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 - 10.1046/j.0953-816x.2001.01614.x
Subject(s) - protein kinase c , protein kinase a , endocrinology , medicine , hyperalgesia , epinephrine , hormone , second messenger system , kinase , knockout mouse , chemistry , nociception , receptor , biochemistry
We have evaluated the contribution of differences in second messenger signalling to sex differences in inflammatory pain and its control by sex hormones. In normal male but not female rats, epinephrine‐induced mechanical hyperalgesia was antagonized by inhibitors of protein kinase Cε (PKCε), protein kinase A (PKA) and nitric oxide synthetase (NOS). Similarly, in PKCε knockout mice, a contribution of PKCε to epinephrine‐dependent mechanical hyperalgesia occurred in males only. In contrast, hyperalgesia induced by prostaglandin E 2 , in both females and males, was dependent on PKA and NO. In both sexes, inhibitors of mitogen‐activated protein kinase/extracellular‐signal related kinase kinase (MEK) inhibited epinephrine hyperalgesia. In gonadectomized females, the second messenger contributions to epinephrine hyperalgesia demonstrated the pattern seen in males. Administration of oestrogen to gonadectomized females fully reconstituted the phenotype of the normal female. These data demonstrate gender differences in PKCε, PKA and NO signalling in epinephrine‐induced hyperalgesia which are oestrogen dependent and appear to be exerted at the level of the β‐adrenergic receptor or the G‐protein to which it is coupled.