Researchers have discovered a hormonal mechanism in hamsters that connects short winter days with increased aggression in females and differs from one that controls the same response in males.
The discovery, which advances basic knowledge on the connection between certain sex hormones and aggression, could lead to better treatment of inappropriate aggression in humans.
“This study reveals a ripe area for research,” says lead author Nikki Rendon, a PhD student working in the lab of Gregory Demas, professor of biology at Indiana University. “The results show for the first time that melatonin acts directly on the adrenal glands in females to trigger a ‘seasonal aggression switch’ from hormones in the gonads to hormones in the adrenal glands—a major contrast to how this mechanism works in males.”
Earlier research found that wintertime aggression in hamsters arises not from sex hormones in the gonads—ovaries in females and testes in males, which grow less active during shorter days—but rather the adrenal glands, located at the top of the kidneys.
Melatonin in winter
Melatonin is a hormone that rises in the body during darkness and lowers during daylight. The hormone from the adrenal gland is dehydroepiandrosterone, or DHEA, a sex steroid shown to affect aggression levels in mammals and birds, and possibly humans. Professional sports competitions have banned the use of DHEA in athletes.
In another previous study, researchers found that melatonin—in concert with a hormone secreted by the brain’s pituitary gland called adrenocorticotropic, or ACTH—increases the output and enhances the effects of DHEA from adrenal glands in males.
In contrast, the new study reveals that melatonin acts directly on the adrenal glands in females to trigger the release of DHEA, without the need for the pituitary hormone.
DHEA can be converted to androgens and estrogens, which affect aggression in both males and females. In females, DHEA appears to compensate for low levels of estradiol—a form of estrogen—that occurs during the winter.
Evolutionarily, wintertime aggression may confer an advantage during periods of scarce food.
“This study, which builds upon our previous work investigating the connection between short days and aggression in males, shows noteworthy hormonal mechanisms in females and provides important new insights into the role of sex in these mechanisms,” Demas says.
The research, published in the Proceedings of the Royal Academy B, was conducted using Siberian hamsters, or Phodopus sungorus, a species with a similar adrenal system to humans. About 130 hamsters were exposed to long days for a week, after which 45 were exposed to shorter days for 10 weeks. A random subset also received an injection of ACTH.
A highly territorial species, the hamsters were then placed in situations where one hamster was perceived as an intruder into the other’s territory, sparking aggressive actions and short physical fights. The scientists then tracked certain actions, such as the time until an attack, the number of attacks and the length of the attacks, to assign an “aggression score.”
The female hamsters exposed to shorter days had increased levels of both melatonin and DHEA—and higher aggression scores—along with physical changes in their adrenal glands.
Females exposed to longer days did not experience these changes, including those that had received an injection of ACTH, which is known to trigger the release of DHEA.
Collectively, the results show that melatonin is the primary regulator of aggression in females.
“It’s growing increasingly clear that sex hormones play an important role in controlling aggression in both males and females—but females, human and non-human, are traditionally vastly understudied in the sciences,” Rendon says. “By conducting this research on females, we are increasing our understanding of hormones and social behavior in a field currently dominated by discussions on testosterone regulating aggression in males.”
The National Science Foundation, National Institutes of Health, and Indiana University supported the work.
Source: Indiana University