Estrogenic encounters: How interactions between aromatase and the environment modulate aggression

Abstract

Initial investigations into the mechanistic basis of aggression focused on the role of testosterone (T) and a variety of studies on non-human animals found that elevated T levels promote aggression. However, many correlational studies have not detected a significant association between aggression and peripheral T levels. One reason for this inconsistency may be due to differential metabolism of T within the brain, in particular, the conversion of T to estrogen by aromatase. Thus, differences in aromatase enzyme activity, estrogen receptor expression, and related cofactors may have important effects on how steroids affect aggressive behavior. Hormone manipulation studies conducted in a wide variety of species indicate that estrogens modulate aggression. There is also growing evidence that social experience has important effects on the production of estrogen within the brain, and some cases can not be explained by androgenic regulation of aromatase. Such changes in central aromatase activity may play an important role in determining how social experiences affect the probability of whether an individual engages in aggressive behavior. Although studies have been conducted in many taxa, there has been relatively little integration between literatures examining aggression in different species. In this review, we compare and contrast studies examining aggression in birds, mammals, and humans. By taking an integrative approach to our review, we consider mechanisms that could explain species differences in how estrogen modulates aggression.

Rapid effects of estradiol on male aggression depend on photoperiod in reproductively non-responsive mice

“…The effects of estrogens on male aggression are variable, increasing aggression in some species and decreasing aggression in others (Trainor et al, 2006b). This could reflect differences in the expression of estrogen receptor (ER) subtypes.…”

Photoperiod reverses the effects of estrogens on male aggression via genomic and nongenomic pathways

“…These interactions may generate apparent inconsistencies in relationships between neurochemical systems and behavior (2). For example, in most birds and domesticated mice estrogens increase aggression, whereas estrogens decrease aggression or its components in Bluebanded gobies, California mice, and humans (3). This complexity in estrogenic modulation of aggression could be mediated by several factors including differential expression of estrogen receptor (ER) subtypes or differences in receptor activity after estrogen binding.…”

The effects of surgical and chemical castration on intermale aggression, sexual behaviour and play behaviour in the male ferret (Mustela putorius furo)

“…Demas et al, 1999), however, it was found that surgical castration did not reduce aggression. Part of the ineffectiveness of surgical castration might be attributed to species differences, seasonality and age of castration (Trainor et al, 2006). Our findings raise an interesting additional point as in contrast to surgical castration, chemical castration with deslorelin did have an effect on aggression.…”

“…Our findings raise an interesting additional point as in contrast to surgical castration, chemical castration with deslorelin did have an effect on aggression. One of the most likely explanations is that deslorelin as a GnRH agonist decreases the plasma estradiol level, which is also involved in the regulation of aggression (Trainor et al, 2006). Additionally, surgical castration may lead to elevated GnRH and LH levels in the blood, which may result in some testosterone-related compound production in tissues other than the testes.…”