It is widely believed that pain affects men and women differentially; females demonstrate significantly higherbehavioral responses to chronic and inflammatory pain than males. Sex differences in the experiences ofpain reside in part in intrinsic biological differences; i.e., changes in pain responses associated withphysiological fluctuations of gonadal hormones are indicative of a significant contribution of estrogen andprogesterone to the regulation of pain responses. We have recently shown that in female rats estrogenproduces a persistent analgesic effect on injury (inflammation)-induced pain. Our long-term goal is todetermine whether fluctuations during different stages of the female reproductive cycle in inflammatory andpersistent pain perception are due to fluctuations in estrogen. The objective of this proposal is to determine ifestrogen's analgesic effects on inflammatory/chronic pain are mediated through activation of inflammatorymechanisms. Specifically, we hypothesize that estrogen's antihypera'nalgesic effects on injury(inflammation)-induced pain are mediated through up-regulation of corticosterone release which in turndown-regulates COX-2 protein activity and, thus, prostaglandin-biosynthesis. Studies addressing behavioralresponses 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 systemhas been little studied.
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