About this item:

177 Views | 152 Downloads

Author Notes:

Corresponding author: jennifer.rose.merritt@emory.edu (J.R. Merritt).

The authors would like to thank Sarah Heimovics, Cathy Ma, and Carlos Rodriguez-Saltos for technical assistance and Rashidat Ayantunji for animal care.

We are grateful to the Emory University Department of Biology for use of facilities and equipment.

Subjects:

Research Funding:

This work was supported by the National Institutes of Health [R01MH082833, NIH 1R21NIMH102677] and the National Science Foundation [IOS1627789] to DLM, and the Canadian Institutes of Health [133606] to KKS.

Keywords:

  • Aggression
  • Animals
  • Behavior, Animal
  • Brain
  • Dominance-Subordination
  • Estradiol
  • Estrogen Receptor alpha
  • Genotype
  • Male
  • Parenting
  • Polymorphism, Genetic
  • Social Behavior
  • Sparrows

Rapid effects of estradiol on aggression depend on genotype in a species with an estrogen receptor polymorphism

Tools:

Journal Title:

Hormones and Behavior

Volume:

Volume 98

Publisher:

, Pages 210-218

Type of Work:

Article | Post-print: After Peer Review

Abstract:

The white-throated sparrow (Zonotrichia albicollis) represents a powerful model in behavioral neuroendocrinology because it occurs in two plumage morphs that differ with respect to steroid-dependent social behaviors. Birds of the white-striped (WS) morph engage in more territorial aggression than do birds of the tan-striped (TS) morph, and the TS birds engage in more parenting behavior. This behavioral polymorphism is caused by a chromosomal inversion that has captured many genes, including estrogen receptor alpha (ERα). In this study, we tested the hypothesis that morph differences in aggression might be explained by differential sensitivity to estradiol (E2). We administered E2 non-invasively to non-breeding white-throated sparrows and quantified aggression toward a conspecific 10 min later. E2 administration rapidly increased aggression in WS birds but not TS birds, consistent with our hypothesis that differential sensitivity to E2 may at least partially explain morph differences in aggression. To query the site of E2 action in the brain, we administered E2 and quantified Egr-1 expression in brain regions in which expression of ERα is known to differ between the morphs. E2 treatment decreased Egr-1 immunoreactivity in nucleus taeniae of the amygdala, but this effect did not depend on morph. Overall, our results support a role for differential effects of E2 on aggression in the two morphs, but more research will be needed to determine the neuroanatomical site of action.

Copyright information:

© 2018 Elsevier Inc.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Creative Commons License

Export to EndNote