Infanticide: Accounting for genetic variation in mice

Svare, Bruce; Kinsley, Craig Howard; Mann, Martha A.; Broida, John

doi:10.1016/0031-9384(84)90024-6

Cited by 47 publications

(25 citation statements)

References 60 publications

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“…Differentiation of sexually dimorphic nuclei within the brain begins during the 16th to 18th week of fetal development, when males are experiencing a peak in both testosterone production and testosterone uptake by the hypothalamus (Abramovich and Rowe 1973;Smail et al 1981;Finegan et al 1989). This differentiation results from the actions of estrogens produced locally by the aromatisation of testosterone at the site of action (Lephart et al 2001;MacLusky and Naftolin 1981;Naftolin and MacLusky 1984;MacLusky et al 1994;Svare et al 1984). If the influence of the less sensitive AR genes is to result in more testosterone production then the elevated levels may exert a stronger influence on sexual differentiation through estrogen receptors after aromatization in the brain.…”

Section: Discussionmentioning

confidence: 99%

Aggression, Digit Ratio and Variation in Androgen Receptor and Monoamine Oxidase A Genes in Men

2010

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Variation in prenatal exposure to androgens is thought to be responsible for some of the individual differences in aggressive behavior among adults. A putative indicator of prenatal testosterone exposure, 2D:4D (the index to ring finger length) ratios have shown a weak correlation with aggression. Variation in sensitivity of the androgen receptor, resulting from polymorphism in the AR gene, is also thought to influence the relative expression of sexually dimorphic traits within each sex, including aggressive behavior and 2D:4D. Here we examine variation in aggression, 2D:4D, and polymorphism in the AR and MAO-A genes in a sample of 188 men. We find no evidence of AR gene influence on right hand 2D:4D, and a weak trend towards more feminine-typical left hand 2D:4D in men with more sensitive androgen receptors. Men with more sensitive androgen receptors tended to score lower on many of the subscales of the Aggression Questionnaire and Indirect Aggression Questionnaire. We found no influence of MAO-A allele on either digit ratio or aggressive behavior. We conclude that more masculine-typical 2D:4D does not reflect greater sensitivity to testosterone through variation in this locus on the AR gene, and that AR alleles conferring greater sensitivity to testosterone are associated with lower, not higher propensity to aggression.

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Section: Discussionmentioning

confidence: 99%

Aggression, Digit Ratio and Variation in Androgen Receptor and Monoamine Oxidase A Genes in Men

2010

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“…A similar paradoxical effect of fetal androgen exposure is seen on a behavioral trait: Infanticide in mice. Males are more infanticidal than females, yet increased fetal testosterone exposure lowers propensity to infanticide (Svare et al, 1984). Male gerbils are more likely to use their right paws for support than females; treatment with androgens at 4 days of age produces a more feminine typical posture at adulthood (Clark, Robertson, & Galef, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…The local-effects hypothesis (McFadden, 2002) posits that variation in number of androgen receptors in different target tissues, or localized variation in aromatase activity and/or 5-reductase, influences the semi-independent masculinization of different regions, and thus of different traits. Differentiation of sexually dimorphic nuclei within the brain appears to be due largely to estrogens that are aromatized from testosterone at the site of action (Lephart et al, 2001;MacLusky et al, 1994;Svare et al, 1984). The aromatization hypothesis (MacLusky & Naftolin, 1981;Naftolin & MacLusky, 1984) predicts that masculinization may result from estrogen exposure, as well as androgen exposure.…”

Section: Discussionmentioning

confidence: 99%

“…The aromatization hypothesis (MacLusky & Naftolin, 1981;Naftolin & MacLusky, 1984) predicts that masculinization may result from estrogen exposure, as well as androgen exposure when masculinization is driven by estrogen locally aromatized from testosterone in the target tissue. Differentiation of sexually dimorphic nuclei within the brain appears to be due to such a mechanism (Lephart, Lund, & Horvath, 2001;MacLusky, Walters, Clark, & Toran-Allerand, 1994;Svare, Kinsley, Mann, & Broida, 1984).…”

Section: Introductionmentioning

confidence: 99%

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Intrauterine Position Effects on Anogenital Distance and Digit Ratio in Male and Female Mice

et al. 2007

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Anogenital distance (AGD) and the ratio of the second (index) to fourth (ring) digit lengths (2D:4D) are two widely used indicators of prenatal androgen exposure. The former is commonly used in rodent models, while the latter is principally used in human studies. We investigated variation in these two traits in C57BL/6J mice to test the hypothesis that variation in these two traits reflect a common underlying variable, presumably testosterone exposure. AGD is a sexually dimorphic trait used to sex young rodents. This distance typically increases and becomes more male-like in female pups when their uterine neighbors are male. 2D:4D is sexually dimorphic in a number of species, including humans and other great apes. Lower digit ratios may be associated with greater exposure to androgens during fetal development in humans. We found the expected sexual dimorphism in AGD, but no significant sex difference in 2D:4D, and no correlation between 2D:4D and AGD. Gestating next to males increased a pup's 2D:4D ratio, but it had no effect on AGD. The lack of correlation between 2D:4D and AGDs in this mouse strain suggests that these two measures do not reflect a common influence of androgen exposure. The possible roles of temporal and localized effects of masculinization are discussed.

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“…Maternal aggression includes both defensive and offensive elements; lactating females engage in defensive attacks toward males and offensive attacks toward female intruders (Parmigiani et al, 1989; Lucion and de Almeida, 1996; de Almeida et al this volume). In some respects, infanticide (Svare et al, 1984), predatory aggression, such as mouse killing behavior by rats (Karli et al, 1972), and play fighting in juvenile rats and hamsters (Pellis and Pellis, 1988; Pellis and Iwaniuk, 2000) also qualify as aggressive behavior. However, these are considered to be qualitatively different from offensive or defensive aggression.…”

Section: Rodent Models For Aggressive Behaviormentioning

confidence: 99%

Neurogenetics of Aggressive Behavior: Studies in Rodents

Takahashi

Miczek

2013

Current Topics in Behavioral Neurosciences

185

132

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Aggressive behavior is observed in many animal species, such as insects, fish, lizards, frogs, and most mammals including humans. This wide range of conservation underscores the importance of aggressive behavior in the animals’ survival and fitness, and the likely heritability of this behavior. Although typical patterns of aggressive behavior differ between species, there are several concordances in the neurobiology of aggression among rodents, primates, and humans. Studies with rodent models may eventually help us to understand the neurogenetic architecture of aggression in humans. However, it is important to recognize the difference between the ecological and ethological significance of aggressive behavior (species-typical aggression) and maladaptive violence (escalated aggression) when applying the findings of aggression research using animal models to human or veterinary medicine. Well-studied rodent models for aggressive behavior in the laboratory setting include the mouse (Mus musculus), rat (Rattus norvegicus), hamster (Mesocricetus auratus), and prairie vole (Microtus ochrogaster). The neural circuits of rodent aggression have been gradually elucidated by several techniques e.g. immunohistochemistry of immediate-early gene (c-Fos) expression, intracranial drug microinjection, in vivo microdialysis, and optogenetics techniques. Also, evidence accumulated from the analysis of gene-knockout mice shows the involvement of several genes in aggression. Here we review the brain circuits that have been implicated in aggression, such as the hypothalamus, prefrontal cortex (PFC), dorsal raphe nucleus (DRN), nucleus accumbens (NAc), and olfactory system. We then discuss the roles of glutamate and γ-aminobutyric acid (GABA), major inhibitory and excitatory amino acids in the brain, as well as their receptors, in controlling aggressive behavior, focusing mainly on recent findings. At the end of this chapter, we discuss how genes can be identified that underlie individual differences in aggression, using the so-called forward genetics approach.

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Infanticide: Accounting for genetic variation in mice

Cited by 47 publications

References 60 publications

Aggression, Digit Ratio and Variation in Androgen Receptor and Monoamine Oxidase A Genes in Men

Aggression, Digit Ratio and Variation in Androgen Receptor and Monoamine Oxidase A Genes in Men

Intrauterine Position Effects on Anogenital Distance and Digit Ratio in Male and Female Mice

Neurogenetics of Aggressive Behavior: Studies in Rodents

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