Differential expression of hypothalamic genes in juncos (Junco hyemalis) during gonadal development implications for regulation of timing of breeding


Meeting Abstract

P2-31  Friday, Jan. 5 15:30 – 17:30  Differential expression of hypothalamic genes in juncos (Junco hyemalis) during gonadal development: implications for regulation of timing of breeding ANDERSON-BUCKINGHAM, S*; BAUER, C; FUDICKAR, A; ABOLINS-ABOLS, M; ATWELL, J; KETTERSON, E; GREIVES, T; North Dakota State Univ.; Adelphi Univ.; Indiana Univ.; Indiana Univ.; Indiana Univ.; Indiana Univ.; North Dakota State Univ. cbauer@adelphi.edu

Seasonally breeding birds must time their reproduction to match optimal environmental conditions. The transition into breeding condition and gonadal growth are regulated by the hypothalamic-pituitary-gonadal (HPG) axis at multiple levels. Our study focuses on the level of the hypothalamus and examines expression of candidate genes in relation to three potential mechanisms regulating gonadal recrudescence: 1) top-down stimulation and inhibition of the HPG-axis via gonadotropin-releasing hormone (GnRH) and gonadotropin-inhibitory hormone (GnIH), 2) sex steroid negative feedback sensitivity via androgen receptor (AR) and estrogen receptor alpha (ERα), and 3) sensitivity to stress hormones via glucocorticoid receptor (GR) and mineralocorticoid receptor (MR). We measured hypothalamic mRNA expression of these genes via qPCR in captive male Dark-eyed Juncos (Junco hyemalis) held under the same conditions but expressing different stages of gonadal recrudescence in early spring. All males were captured from the same overwintering population, but males from a resident subspecies were in a more advanced stage of gonadal recrudescence than males from a migratory subspecies. We found that residents had significantly higher mRNA expression levels of GnRH, lower levels of AR and ERα, and similar levels of GR and MR. These results suggest decreased hypothalamic sensitivity to sex steroid negative feedback and increased GnRH production as factors promoting gonadal recrudescence.

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