In particular, a dramatic increase in publications began in the mid-1990s, which may be attributable to several influential review articles along with other events occurring in the 1990s that drew considerable attention to the topic. In 1992, an important publication by Karen Berkley32 highlighted the importance of sex-related issues in neuroscience research. Thus, the early to mid-1990s was a period of increased scholarly activity regarding sex differences in pain. Another neurotransmitter system that could contribute to sex differences in pain responses is the dopaminergic system.
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Next, we will review recent findings regarding sex differences in experimental pain sensitivity. Many studies have investigated the prevalence of musculoskeletal pain in men and women, with some assessing chronic musculoskeletal pain irrespective of the site, whereas others have been site specific. In a previous review, Rollman and Lautenbacher341 concluded that women have greater frequency of musculoskeletal pain than men.
In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids.[157] In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone. Because testicular differentiation occurs without SRY in approximately 20% of individuals with 46,XX testicular DSD, there might be other important genes that cause 46,XX testicular DSD19). SOX9 on chromosome 17q24.3 is one of the genes that plays an important role in the development of the skeleton and genital organs4).
