Sex Differences in Capsaicin-Induced Nocifensive Responses and Thermal Hyperalgesia in Rats

• Main Authors: Yu-Ching Lu, 呂雨青
• Other Authors: Fong-Sen Wu
• Format: Others
• Language: en_US
• Published: 2006
• Online Access: http://ndltd.ncl.edu.tw/handle/27036221173028131300

碩士 === 國立成功大學 === 生理學研究所 === 94 === Previous studies from our laboratory have demonstrated that the male sex steroid testosterone inhibits slightly, but the female sex steroid 17b-estradiol (E2) potentiates dramatically, the capsaicin receptor-mediated current in male rat dorsal root ganglion neurons. These findings, together with recent clinical observation that women experience capsaicin-induced pain as more intense than men do, suggest that sex differences in pain perception result from differential modulation of the capsaicin receptor by different sex steroids. However, it is unclear whether sex differences in capsaicin-induced pain also occur in rats. In the present study, we used pharmacological methods and nociceptive behavioral tests to determine whether there are sex differences in capsaicin-induced nocifensive behaviors and thermal hyperalgesia in rats in vivo and to explore the mechanism underlying these sex differences. Our results revealed that the capsaicin-induced nocifensive response was significantly greater in female rats than in male rats. Moreover, the enhanced female sensitivity to the capsaicin-induced nocifensive response was completely reversed by ovariectomy (OVX) operated 6 weeks prior to capsaicin injection. Importantly, intradermal injection of E2, but not progesterone potentiated the capsaicin-induced nocifensive response in OVX rats. Similarly, E2 intradermally injected into male rat handpaws dose-dependently enhanced the capsaicin-induced nocifensive response. Sex difference also occurs in capsaicin-induced thermal hyperalgesia, with female rats being greater and longer than male rats. Furthermore, in female rats, capsaicin induced lesser and shorter heat hyperalgesia after OVX compared to sham surgery. In addition, E2 but not progesterone replacement reversed attenuation of capsaicin-induced thermal hyperalgesia in OVX rats. Together, these results suggest that E2 mediates the enhanced sensitivity in female rats to capsaicin-induced nociception and thermal hyperalgesia, consistent with an interaction between E2 and capsaicin receptors in modifying pain perception.