SNRP at Hunter College

人们普遍认为，疼痛对男性和女性的影响不同;女性表现出显着更高的 行为反应慢性和炎症疼痛比男性。性别差异的经验， 疼痛部分地存在于内在的生物学差异中;即，疼痛反应的变化与 性腺激素的生理波动表明雌激素的重要作用， 孕酮调节疼痛反应。我们最近发现雌性大鼠的雌激素 对损伤（炎症）引起的疼痛产生持续的镇痛作用。我们的长期目标是 确定在女性生殖周期的不同阶段，炎症和 持续的疼痛感是由于雌激素的波动。本提案的目的是确定， 雌激素对炎性/慢性疼痛的镇痛作用是通过激活炎性 机制等具体地说，我们假设雌激素对损伤的抗痛觉过敏作用 （炎症）诱导的疼痛是通过上调皮质酮的释放， 下调考克斯-2蛋白活性，从而下调野牡丹素生物合成。针对行为的研究 女性对疼痛的反应和雌激素在持续性/炎性疼痛中的作用是有限的。 此外，尽管一些出版物研究了雌激素对卵巢组织中考克斯-2的影响， 雌激素在外周和中枢神经系统前列腺素释放调节中的作用 很少被研究。

It is widely believed that pain affects men and women differentially; females demonstrate significantly higher behavioral responses to chronic and inflammatory pain than males. Sex differences in the experiences of pain reside in part in intrinsic biological differences; i.e., changes in pain responses associated with physiological fluctuations of gonadal hormones are indicative of a significant contribution of estrogen and progesterone to the regulation of pain responses. We have recently shown that in female rats estrogen produces a persistent analgesic effect on injury (inflammation)-induced pain. Our long-term goal is to determine whether fluctuations during different stages of the female reproductive cycle in inflammatory and persistent pain perception are due to fluctuations in estrogen. The objective of this proposal is to determine if estrogen's analgesic effects on inflammatory/chronic pain are mediated through activation of inflammatory mechanisms. Specifically, we hypothesize that estrogen's antihypera'nalgesic effects on injury (inflammation)-induced pain are mediated through up-regulation of corticosterone release which in turn down-regulates COX-2 protein activity and, thus, prostaglandin-biosynthesis. Studies addressing behavioral responses to pain in females and the role of estrogen in persistent/inflammatory pain are limited. Furthermore, although several publications have studied the effects of estrogen on COX-2 in ovarian tissue, the role of estrogen in the regulation of prostaglandin release in the peripheral and central nervous system has been little studied.