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Seasonal patterns of melatonin alter aggressive phenotypes of female Siberian hamsters

Citation

Rendon, Nikki et al. (2020), Seasonal patterns of melatonin alter aggressive phenotypes of female Siberian hamsters, Dryad, Dataset, https://doi.org/10.5061/dryad.j0zpc86c6

Abstract

Many animal species exhibit year-round aggression, a behaviour that allows individuals to compete for limited resources in their environment (e.g., food and mates).
Interestingly, this high degree of territoriality persists during the non-breeding season, despite low levels of circulating gonadal steroids (i.e., testosterone [T] and oestradiol
[E2]). Our previous work suggests that the pineal hormone melatonin mediates a ‘seasonal switch’ from gonadal to adrenal regulation of aggression in Siberian hamsters
(Phodopus sungorus); solitary, seasonally breeding mammals that display increased aggression during the short, ‘winter-like’ days (SDs) of the non-breeding season. To test
the hypothesis that melatonin elevates non-breeding aggression by increasing circulating and neural steroid metabolism, we housed female hamsters in long days (LDs)
or SDs, administered them timed or mis-timed melatonin injections (mimic or do not mimic a SD-like signal, respectively), and measured aggression, circulating hormone
profiles, and aromatase (ARO) immunoreactivity in brain regions associated with aggressive or reproductive behaviours (paraventricular hypothalamic nucleus [PVN],
periaqueductal gray [PAG], and ventral tegmental area [VTA]). Females that were responsive to SD photoperiods (SD-R) and LD females given timed melatonin injections
(Mel-T) exhibited gonadal regression and reduced circulating E2, but increased aggression and circulating dehydroepiandrosterone (DHEA). Furthermore, aggressive challenges differentially altered circulating hormone profiles across seasonal phenotypes; reproductively inactive females (ie, SD-R and Mel-T females) reduced circulating
DHEA and T, but increased E2 after an aggressive interaction, whereas reproductively active females (i.e., LD females, SD non-responder females, and LD females given mis-timed melatonin injections) solely increased circulating E2. Although no differences in neural ARO abundance were observed, LD and SD-R females showed distinct associations between ARO cell density and aggressive behaviour in the PVN, PAG, and VTA. Taken together, these results suggest that melatonin increases non-breeding
aggression by elevating circulating steroid metabolism after an aggressive encounter and by regulating behaviourally relevant neural circuits in a region-specific manner.

Funding

National Institute of Mental Health, Award: R21MH109942

National Institute of Child Health and Human Development, Award: T32HD049336

Division of Integrative Organismal Systems, Award: IOB-0543798

Division of Integrative Organismal Systems, Award: IOS-1406063