title: Post-hatch oral estrogen in zebra finches (Taeniopygia guttata): is infertility due to disrupted testes morphology or reduced copulatory behavior?
abstract: Previous studies show that post-hatch oral exposure of zebra finches to estradiol benzoate compromises male fertility, but the basis of the infertility is not clear. In this study, zebra finch nestlings were orally dosed with estradiol benzoate (at 1, 10, or 100 nmol/g BW per day, post-hatch days 5 to 11 [EB1, EB10, and EB100, respectively]). EB10 and EB100 males exhibited no significant differences in the frequency of mounting behavior (compared to canola oil [vehicle]-treated controls), when observed for six weeks as adults in communal breeding cages with similarly treated females; EB1 males showed reduced mounting behavior compared to controls (p<0.05). EB- and control-treated adult pairs were subsequently co-housed in a communal breeding trial to determine the extent of parentage outside the established pair-bond. Microsatellite analysis was consistent with EB-treated males having lower success than controls in obtaining paternity outside the established pair-bond. Histological examination of testes revealed dose-related disruption of normal morphology: disrupted basal-to-lumen laminarity of spermatogenesis stages, increased vacuolization within seminiferous tubules, decreased sperm aggregation and decreased spermatid density. Additionally, EB100 and control males were housed individually, implanted with testosterone propionate (TP) and presented with a female 3, 5, 9, and 11 days post-implantation for assessment of male sexual behavior. EB-treated, TP-implanted birds showed a slight decrease in mounting and singing behavior on day 5 after implantation; other male courtship behaviors (display, solicitation) were unaffected. Taken together, these results suggest that infertility in male zebra finches resulting from early oral estrogen exposure is more likely due to disrupted testicular morphology than altered sexual behavior.
authors.affiliation: Department of Animal Science, University of California, Davis, USA. johanna.rochester@colorado.edu
authors.forename: Johanna R
authors.initials: JR
authors.lastname: Rochester
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Forstmeier
authors.forename: James R
authors.initials: JR
authors.lastname: Millam
mesh_terms: D000284:Administration, Oral; D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001715:Bird Diseases / Q000139:chemically induced / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D052244:Endocrine Disruptors / Q000008:administration & dosage*; D004958:Estradiol / Q000008:administration & dosage / Q000031:analogs & derivatives*; D005260:Female; D046369:Finches / Q000502:physiology*; D007248:Infertility, Male / Q000139:chemically induced* / Q000503:physiopathology; D008297:Male; D010334:Paternity; D012726:Sexual Behavior, Animal / Q000187:drug effects*; D013091:Spermatogenesis / Q000187:drug effects*; D018709:Statistics, Nonparametric; D013737:Testis / Q000187:drug effects / Q000254:growth & development
chemical_list: D052244:Endocrine Disruptors; C074283:estradiol 3-benzoate; D004958:Estradiol