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**Claims Related to Anti Trans Legislation **

See:

https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2017.00632/full

"sexual differentiation of the gonad is dependent upon the Y chromosome and the SRY/Sry gene. However, brain sexual differentiation is generally orchestrated by a surge in gonadal steroid hormones during embryo development followed by a second surge later in adulthood. This paradigm is considered “organization-activational programming” and occurs in a sex-specific manner (Phoenix et al., 1959; Arnold and Breedlove, 1985; Morris et al., 2004). The organizational-activational concept was formulated based initially on findings in guinea pigs (Cavia porcellus). Female guinea pigs prenatally exposed to testosterone propionate during a specific developmental window had permanent rewiring of the neural circuitry and as adults, demonstrated male-pattern behaviors (Phoenix et al., 1959). Similar results were then obtained with other mammals (Phoenix et al., 1959; Arnold and Breedlove, 1985; Morris et al., 2004). The early brain programming is termed the organizational period and is characterized by spikes in androgens and/or estrogens such that the brain becomes permanently masculinized (Watson and Adkins-Regan, 1989a,b; Bowers et al., 2010; Konkle and McCarthy, 2011). In the developing mouse brain, sex chromosomes appear to interact with steroid hormones to increase the expression of aromatase expression, which converts androgens into estrogens, and this process appears to be through activation of neural estrogen receptor β (ESR2) (Cisternas et al., 2015, 2017). Masculinization of several brain regions, including the hippocampus, requires aromatization of testosterone to estrogen (Watson and Adkins-Regan, 1989a,b; Bowers et al., 2010; Konkle and McCarthy, 2011). Programming of the male brain though requires both defeminization and masculinization, which generally requires binding of estradiol to its cognate receptors, estrogen receptor-α (ESR1) and ESR2 (Naftolin et al., 1975; Lephart, 1996; McCarthy, 2010). MRI examination of the brain from women with androgen insensitivity syndrome (CAIS), who exhibit a male (46,XY) karyotype but lack functional androgen receptors, reveals that testosterone alone may, however, regulate development of certain brain regions (Savic et al., 2017). These include the somatosensory and visual cortices and their axonal connections to the frontal cortex, along with the connections from the amygdala.

For characteristic sex-dependent behaviors, especially those seen in males, a second spike in steroid hormones at adulthood (“activational period”) is required for full elaboration of sex-specific neurobehavioral pathways (Tsai et al., 2009; Menger et al., 2010; Nugent and McCarthy, 2011; Jasarevic et al., 2012; Matsuda et al., 2012; Chung and Auger, 2013). Steroid hormones at both periods may trigger epigenetic changes in various brain regions that underpin sex differences in brain responses (Tsai et al., 2009; Menger et al., 2010; Nugent and McCarthy, 2011; Jasarevic et al., 2012; Matsuda et al., 2012; Chung and Auger, 2013). However, the question remains as to potential other contributions of sex chromosomes and those genes residing on the X and Y in initiating brain sexual differentiation. One gene residing on the Y chromosome that that has received particular attention is SRY (in men)/Sry (in other therian mammals). For consistency, the gene annotation form Sry will be used throughout the manuscript, unless studies within humans or the human form of SRY are being described."

https://www.nature.com/articles/s41380-018-0198-y

https://www.nature.com/articles/s41380-018-0198-y/figures/1

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