Involvement of Estrogen in Rapid Pain Modulation in the Rat Spinal Cord

摘要: The pivotal role of estrogens in the pain sensitivity has been investigated many ways. Traditionally, it is ascribed to slow genomic changes mediated by classical nuclear estrogen receptors (ER), ERα and ERβ, depending on peripheral estrogens. Recently, become clear that can also signal through membrane ERs (mERs), such as G-protein-coupled ER1 (GPER1), mediating non-genomic effects. However, spinal specific played underlying cellular mechanisms remain elusive. present study rapid estrogenic regulation nociception at level. Spinal administration 17β-estradiol (E2), most potent natural estrogen, acutely produced a remarkable mechanical allodynia thermal hyperalgesia without significant differences among male, female ovariectomized (Ovx) rats. E2-induced pro-nociceptive effects were partially abrogated ICI 182,780 (ERs antagonist), mimicked E2-BSA (a mER agonist). Inhibition local E2 synthesis 1,4,6-Androstatrien-3,17-dione (ATD, irreversible aromatase inhibitor), or blockade an inhibitory effect late phase formalin nociceptive responses. Notably, lumbar puncture injection G15 selective GPER1 antagonist) resulted similar but more efficient inhibition responses compared with 182,780. At level, amplitude decay time spontaneous postsynaptic currents attenuated short treatment slices. These results indicate facilitates transmission cord via activation membrane-bound receptors.