SNRP at Hunter College

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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.