title: Effects of male and female sex steroids on the development of normal and the transient Froriep's dorsal root ganglia of the chick embryo.
abstract: Sex steroids can influence developmental processes and support the survival of neurons in the embryonic central nervous system. Recent studies have shown that estrogen receptors are also expressed in the peripheral nervous system, in the dorsal root ganglia (DRG) of chick embryos. However, no studies have examined the effects of sex steroids on development of embryonic DRG. In the present study, 0.2 microg, 1.0 microg, 5.0 microg 10 microg, 20 microg, 25 microg, and 40 microg doses of testosterone or estradiol were delivered to chick embryos at Hamburger and Hamilton stage 18 (E3). The actions of these doses of sex steroids on the development of the C5DRG (fifth cervical ganglion, a "normal" DRG) and C2DRG (a transient ganglion known as a "Froriep's DRG") were then evaluated by quantifying ganglionic volumes, cell number, proliferation, and apoptosis after 1 day of growth to stage 23. We found that both testosterone and estradiol promoted proliferation of cells in both normal DRG and the Froriep's ganglia. By contrast, estradiol significantly increased the number of apoptotic cells, while testosterone strongly inhibited apoptosis. These actions of sex steroids on DRG development were dose-dependent, and C5DRG and C2DRG showed different sensitivities to the applied sex steroids. In addition, the present results demonstrated that specific ER and AR inhibitors (tamoxifen and flutamide) did not influence the effects of 5 microg E2 and 5 microg T on C2 and C5DRG significantly. These results demonstrate that male and female sex steroids can modulate DRG development through an epigenetic mechanism, as had been shown for the central nervous system.
authors.affiliation: College of Biological Sciences, China Agricultural University, Beijing, 100094, PR China.
authors.forename: Jiali
authors.initials: J
authors.lastname: Liu
authors.forename: Dawei
authors.initials: D
authors.lastname: Chen
authors.forename: Ronald S
authors.initials: RS
authors.lastname: Goldstein
authors.forename: Sheng
authors.initials: S
authors.lastname: Cui
mesh_terms: D000726:Androgen Antagonists / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D019521:Body Patterning / Q000187:drug effects* / Q000502:physiology; D001973:Bromodeoxyuridine; D002452:Cell Count; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D049109:Cell Proliferation / Q000187:drug effects*; D002642:Chick Embryo; D004305:Dose-Response Relationship, Drug; D004628:Embryonic Structures / Q000166:cytology / Q000187:drug effects* / Q000196:embryology; D004958:Estradiol / Q000494:pharmacology; D004965:Estrogen Antagonists / Q000494:pharmacology; D005485:Flutamide / Q000494:pharmacology; D005727:Ganglia, Spinal / Q000166:cytology / Q000187:drug effects* / Q000196:embryology; D012739:Gonadal Steroid Hormones / Q000494:pharmacology*; D009475:Neurons, Afferent / Q000187:drug effects*; D012727:Sex Characteristics; D013629:Tamoxifen / Q000494:pharmacology; D013739:Testosterone / Q000494:pharmacology
chemical_list: D000726:Androgen Antagonists; D004965:Estrogen Antagonists; D012739:Gonadal Steroid Hormones; D013629:Tamoxifen; D013739:Testosterone; D004958:Estradiol; D005485:Flutamide; D001973:Bromodeoxyuridine