Aggression in male mice lacking functional estrogen receptor α.

Scordalakes, Elka M.; Rissman, Emilie F.

doi:10.1037/0735-7044.117.1.38

Cited by 77 publications

(61 citation statements)

References 33 publications

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“…At the time of surgery each mouse received a subcutaneous SILASTIC capsule (1.02 mm inner diameter ϫ 2.16 mm outer diameter) in the midscapular region filled to 10 mm in length with crystalline testosterone (T). These implants yield plasma T levels within the physiological range for C57BL/6J males: 1-2 ng/ml (Scordalakes and Rissman, 2003). About 4 weeks later, at the end of the behavioral testing series, mice were deeply anesthetized with a lethal dose of sodium pentobarbital.…”

Section: Methodsmentioning

confidence: 99%

Sex Chromosome Complement and Gonadal Sex Influence Aggressive and Parental Behaviors in Mice

Gatewood¹,

Wills²,

Shetty³

et al. 2006

J. Neurosci.

220

227

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Across human cultures and mammalian species, sex differences can be found in the expression of aggression and parental nurturing behaviors: males are typically more aggressive and less parental than females. These sex differences are primarily attributed to steroid hormone differences during development and/or adulthood, especially the higher levels of androgens experienced by males, which are caused ultimately by the presence of the testis-determining gene Sry on the Y chromosome. The potential for sex differences arising from the different complements of sex-linked genes in male and female cells has received little research attention. To directly test the hypothesis that social behaviors are influenced by differences in sex chromosome complement other than Sry, we used a transgenic mouse model in which gonadal sex and sex chromosome complement are uncoupled. We find that latency to exhibit aggression and one form of parental behavior, pup retrieval, can be influenced by both gonadal sex and sex chromosome complement. For both behaviors, females but not males with XX sex chromosomes differ from XY. We also measured vasopressin immunoreactivity in the lateral septum, which was higher in gonadal males than females, but also differed according to sex chromosome complement. These results imply that a gene(s) on the sex chromosomes (other than Sry) affects sex differences in brain and behavior. Identifying the specific X and/or Y genes involved will increase our understanding of normal and abnormal aggression and parental behavior, including behavioral abnormalities associated with mental illness.

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Section: Methodsmentioning

confidence: 99%

Sex Chromosome Complement and Gonadal Sex Influence Aggressive and Parental Behaviors in Mice

Gatewood¹,

Wills²,

Shetty³

et al. 2006

J. Neurosci.

220

227

View full text Add to dashboard Cite

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“…Evolutionary conserved genes affecting neurotransmitter signaling and metabolism affect aggressive behavior, including serotonin (18)(19)(20)(21)(22)(23)(24), monoamine oxidase A (25, 26), dopamine (20), octopamine (20,27), nitric oxide (28), and GABA (29). Increased aggression is associated with mutations in androgen and estrogen signaling in vertebrates (30) and sex determination in Drosophila (31,32). Genes involved in brain development or synaptogenesis have been associated with aggression in mice (33) and Drosophila (13,15,20), whereas in humans, quantitative differences in size or structure of the amygdala and prefrontal cortex have been associated with aggression (34).…”

mentioning

confidence: 99%

Complex genetic architecture of Drosophila aggressive behavior

Zwarts

Magwire

Carbone

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Epistasis and pleiotropy feature prominently in the genetic architecture of quantitative traits but are difficult to assess in outbred populations. We performed a diallel cross among coisogenic Drosophila P-element mutations associated with hyperaggressive behavior and showed extensive epistatic and pleiotropic effects on aggression, brain morphology, and genome-wide transcript abundance in head tissues. Epistatic interactions were often of greater magnitude than homozygous effects, and the topology of epistatic networks varied among these phenotypes. The transcriptional signatures of homozygous and double heterozygous genotypes derived from the six mutations imply a large mutational target for aggressive behavior and point to evolutionarily conserved genetic mechanisms and neural signaling pathways affecting this universal fitness trait.

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“…Studies of aggression (15)(16)(17) and anxiety (18) have suggested that ER␣ and ER␤ can have opposing effects on behavior, and we tested whether photoperiod regulation of receptor expression mediated the effect of photoperiod on aggression. Both ER␣ and ER␤ selective agonists increased aggression in short days but decreased aggression in long days, indicating that simple changes in receptor expression could not explain the effect of photoperiod on estrogen-mediated aggression.…”

mentioning

confidence: 99%

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

Trainor

Lin

Finy

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

100

103

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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...

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Aggression in male mice lacking functional estrogen receptor α.

Cited by 77 publications

References 33 publications

Sex Chromosome Complement and Gonadal Sex Influence Aggressive and Parental Behaviors in Mice

Sex Chromosome Complement and Gonadal Sex Influence Aggressive and Parental Behaviors in Mice

Complex genetic architecture of Drosophila aggressive behavior

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

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