【摘 要】
：
Discussions about how estrogen modulates pain sensitivity have largely focused on genomic actions via nuclear receptors, but its rapid effects on synaptic transmission in nociceptive pathways have not
【机 构】
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Institute of Neurobiology, Institutes of Brain Science and State Key Laboratory of Medical Neurobiol
【出 处】
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中国神经科学学会第九届全国学术会议暨第五届会员代表大会
论文部分内容阅读
Discussions about how estrogen modulates pain sensitivity have largely focused on genomic actions via nuclear receptors, but its rapid effects on synaptic transmission in nociceptive pathways have not been elucidated.The present study investigated the role of 17β-estradiol (E2) in the regulation of excitatory postsyrnaptic currents (EPSCs) and long-term potentiation (LTP) in the superficial dorsal horn (SDH, laminae Ⅰ/Ⅱ) using spinal cord slices with attached dorsal root from juvenile (2-3 weeks) rats.EPSCs and LTP of C-fiber evoked field potentials (fEPSPs) were recorded from SDH by stimulating dorsal root (DR) and Lissauers tract (LT) respectively.We found that N-methyl-D-aspartate (NMDA)-induced currents were rapidly and dose-dependently enhanced by bath application of E2, while α-amino-3-hydroxy-5-methyl-4-isoxazolepropri-anate (AMPA)-evoked currents were inhibited.Moreover, short infusion of E2 could induce chemical LTP of NMDA receptor-mediated EPSCs (NMDA-EPSCs) and long-term depression (LTD) of AMPA-EPSCs.In field potential recordings, slices perfused with E2 exhibited a significant enhancement of LTP magnitude compared with control slices which could be mimicked by E2-BSA, an agonist of membrane estrogen receptor (mER).The elevation effect of E2 on LTP ceiling could be prevented by ER antagonist ICI 182,780.These data suggest that estrogen modulates nociception probably by enhancing NMDA receptor-mediated currents or intensifying LTP via mER.
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