Postnatal Germ Cell Development during Mini-Puberty in the Mouse Does Not Require Androgen Receptor: In infants there is a surge of production of pituitary gonadotropins and subsequent androgen production from the testis at about age 3 months. Some suggest that this "mini-puberty" controls the transformation of primitive germ cells into type A spermatogonia, which has prompted routine hormonal therapy in patients with undescended testes in an effort to increase the number of spermatogonia. However, some believe that other mechanisms may play a role which are nonandrogenic. Li et al (page 1361) from Australia used an androgen receptor knockout mouse model to assess the role of androgens in mini-puberty, and found that gonocyte migration and proliferation in the first 10 days of life occurred independent of androgen. They postulate that gonadotropins may act via other non-androgenic factors. It is not yet known if this same phenomenon occurs in humans. Further study is needed to determine if identification of these other factors can help to improve fertility potential in patients with undescended testes.
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