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Despite recent discoveries of the specific contributions of genes to behavior, the molecular mechanisms mediating contributions of the environment are understudied. We demonstrate that the behavioral effects of estrogens on aggression are completely reversed by a discrete environmental signal, day length. Selective activation of either estrogen receptor ␣ or ␤ decreases aggression in long days and increases aggression in short days. In the bed nucleus of the stria terminalis, one of several nuclei in a neural circuit that controls aggression, estrogen-dependent gene expression is increased in long days but not in short days, suggesting that estrogens decrease aggression by driving estrogen-dependent gene expression. Estradiol injections increased aggression within 15 min in short days but not in long days, suggesting that estrogens increase aggression in short days primarily via nongenomic pathways. These data demonstrate that the environment can dictate how hormones affect a complex behavior by altering the molecular pathways targeted by steroid receptors.estrogen receptor ͉ social behavior ͉ Peromyscus polionotus ͉ seasonality G enes code for the molecular machinery that interacts with the environment to regulate behavior. Despite the importance of gene-environment interactions, relatively few studies have explored the mechanistic bases of these processes (1). 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. In male vertebrates estrogens can be produced in the testes or synthesized in the brain from androgens. ERs can modulate physiology and behavior via both genomic and nongenomic pathways (4). Estrogens can alter the transcription of other genes by translocating to the nucleus and binding to estrogen response elements (ERE) or other response elements (5), a process mediated by an array of cofactors (6). Estrogens can also exert a variety of nongenomic effects that may be mediated by unique membrane-bound receptors (7) or the well characterized ER␣ (8) and ER␤ (9). Recent studies suggest ER␣ and ER␤ can be located at the membrane (10) and may facilitate phosphorylation of MAP kinase and CREB (11). Although the transduction of estrogenic signals has been studied intensively, comparatively little is known about how the environment affects estrogen action.Using a discrete environmental signal, day length (photoperiod), we have discovered a striking gene-environment interaction. Similar to other rodents, male beach mice (Peromyscus polionotus) exhibit testicular regression and are more aggressive when housed in winter-like short days (12...

In three genuses and four species of rodents, housing in winter-like short days (8L:16D) increases male aggressive behavior. In all of these species, males undergo short-day induced regression of the reproductive system. Some studies, however, suggest that the effect of photoperiod on aggression may be independent of reproductive responses. We examined the effects of photoperiod on aggressive behavior in California mice (Peromyscus californicus), which do not display reproductive responsiveness to short days. As expected, short days had no effect on plasma testosterone. Estrogen receptor alpha and estrogen receptor beta immunostaining did not differ in the lateral septum, medial preoptic area, bed nucleus of the stria terminalis, or medial amygdala. However, males housed in short days were significantly more aggressive than males housed in long days. Similar to previous work in beach mice (Peromyscus polionotus), estradiol rapidly increased aggression when male California mice were housed in short days but not when housed in long days. These data suggest that the effects of photoperiod on aggression and estrogen signaling are independent of reproductive responses. The rapid action of estradiol on aggression in short-day mice also suggests that nongenomic mechanisms mediate the effects of estrogens in short days.

OBJECTIVE Women and men generally differ in how frequently they engage in other-and self-directed physical violence and may show distinct emotional risk factors for engagement in these high-impact behaviors. To inform this area, we investigated gender differences in the relationship of emotional tendencies (i.e., anger, hostility, and anhedonic depression) that may represent risk for other-directed (i.e., physical fighting, attacking others unprovoked) and self-directed violence (i.e., self-injury, suicide attempts). METHOD The ethnically-diverse sample consisted of 372 adults (252 men and 120 women ages 18–55) with a history of criminal convictions. Facets of emotional risk assessed with the Aggression Questionnaire (Buss & Warren, 2000) and Mood and Anxiety Symptom Questionnaire (Watson et al., 1995) were entered simultaneously as explanatory variables in regression analyses to investigate their unique contributions to other- and self-directed physical violence in men and women. RESULTS Analyses revealed anhedonic depressive tendencies negatively predicted other-directed violence and positively predicted self-directed violence in both men and women, consistent with a model of depression in which aggression is turned inwards (Henriksson et al., 1993). Gender differences, however, emerged for the differential contributions of anger and hostility to other-and self-directed violence. Specifically, trait anger (i.e., difficulty controlling one’s temper) was associated with other-directed violence selectively in men, whereas trait hostility (i.e., suspiciousness and alienation) was associated with self- and other-directed violence among women. CONCLUSIONS The divergent findings for trait anger and hostility underscore the need to examine gender-specific risk factors for physical violence to avoid excluding potentially useful clinical features of these mental health outcomes.