Endogenous gonadal hormones regulate females' behavioral responses to formalin through prostaglandin E2 release.

Introduction: This study aimed to determine if endogenous gonadal hormones affect the intracellular mechanisms in the spinal cord that control inflammatory pain responses.

Methods: We analyzed behavioral responses to, and changes in, serum levels of prostaglandin E2, estradiol, progesterone, and corticosterone after administration of 5% formalin in intact and ovariectomized (OVX) female rats.

Results: OVX females displayed significantly more flinching than did intact females during Phase I, and after formalin administration their corticosterone levels were significantly lower.

Acute and chronic estradiol replacements differentially alter corticosterone and COX-mediated responses to an inflammatory stimulus in female rats.

Introduction: This study aimed to determine whether the previously reported differential effects of estradiol on inflammation-induced behavioral responses are in part explained through differential activation of the corticosterone-cyclooxygenase (CORT-COX) regulatory pathway.

Methods: Prostaglandin E2 (PGE2), COX, and CORT levels were analyzed before and after a formalin administration (1% vs. 5%, representing different intensities of inflammatory stimuli).

Estradiol and progesterone differentially regulate formalin-induced nociception in ovariectomized female rats.

Clinical and preclinical studies have found sex-specific differences in the discrimination and perception of inflammatory stimuli. The emerging picture suggests that the biological basis of these differences resides in the regulatory activity of gonadal hormones in the central nervous system. This study describes the effects of ovarian hormones in inflammatory pain processes.

The role of female gonadal hormones in behavioral sex differences in persistent and chronic pain: clinical versus preclinical studies.

Clinical and preclinical studies have found sex-specific differences in the discrimination and perception of nociceptive stimuli. This article reviews the current literature concerning the biological basis of sex differences in the behavioral response to persistent inflammatory and chronic pain stimuli. The emerging picture from both clinical and preclinical studies suggests that the basis of these differences in nociceptive responses to such stimuli resides in the regulatory activity of gonadal hormones in the central nervous system.

Estradiol administration mediates the inflammatory response to formalin in female rats.

Female rats demonstrate higher pain sensitivity than do males in various nociceptive assays of inflammation. In the present study, we found that estradiol (20%) replacement in ovariectomized rats attenuated the chronic phase of the formalin response but only at high formalin concentrations thought to rely on peripheral inflammation. An inactive isomer of estradiol, alpha-estradiol, failed to result in the same attenuation (P > 0.