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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Blotting, Western, Corticosterone, Cyclooxygenase 1, Cyclooxygenase 2, Dinoprostone, Estradiol, Estrogens, Female, Formaldehyde, Inflammation, Membrane Proteins, Ovariectomy, Pain, Pain Measurement, Progesterone, Rats, Rats, Sprague-Dawley, Spinal Cord, Testosterone.
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Do endogenous gonadal hormones regulate females ' behavioral responses to formalin through prostaglandin E2 release? Context: This study aimed to determine if endogenous gonadal hormones affect the intracellular mechanisms in the spinal cord that control inflammatory pain responses. 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. OVX females displayed significantly more flinching than did intact females during Phase I, and after formalin administration their corticosterone levels were significantly lower. No differences were seen across COX-1 and COX-2 protein expression in the spinal cord of either naive or formalin-treated rats. However, subsequent to formalin a main effect of gonadectomy was seen in prostaglandin E2 levels; OVX animals had significantly lower prostaglandin E2 levels than intact animals.
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These results indicate that in female rats nociceptive responses to formalin are regulated through the levels of prostaglandin E2, an important mediator in inflammation, whereas protein levels of COX-1 and COX-2 play a more limited role. Final Decision: yes