【摘 要】
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A large body of experimental and clinical evidence suggests that estrogen may regulate pain, yet the exact role and the underlying mechanisms of estrogen action in pain remain unresolved.This investig
【机 构】
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Department of Physiology,Shanghai Jiaotong University School of Medicine,Shanghai 200025,China
【出 处】
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International Conference for Physiological Sciences 2012(201
论文部分内容阅读
A large body of experimental and clinical evidence suggests that estrogen may regulate pain, yet the exact role and the underlying mechanisms of estrogen action in pain remain unresolved.This investigation has been conducted to test the hypothesis that estrogen may regulate visceral pain via acting on pain-modulating neurons in the rostral ventromedial medulla (RVM).In the rat, application of 17-β estradiol (E2, 0.1-1 μM) by microinjection (0.5 μL) into the nucleus raphe magnus (NRM) led to marked augmentation of colorectal distension (CRD)-evoked viscero-motor responses (VMR), whereas intracisternal administration of E2 (10 tM, 10 μL) attenuated morphine-induced analgesia.E2 applied by microelectrophoresis was found to activate pain-facilitating ON cells but not pain-inhibiting OFF cells in NRM and in addition ameliorated morphine-induced inhibition of ON cells.Immunohistochemical staining revealed expression of GPR30, a putative membrane receptor for estrogen, in the Golgi apparatus of a portion of spinally-projecting NRM neurons.ERα or ERβ immunoreactivity was not detected in the same region.
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