Stress and the development of agonistic behavior in golden hamsters

Delville, Yvon; David, Jesuye; Taravosh-Lahn, Kereshmeh; Wommack, Joel C.

doi:10.1016/s0018-506x(03)00130-2

Cited by 77 publications

(49 citation statements)

References 59 publications

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“…Given differences in corticosterone between genotype, we cannot rule out a role for glucocorticoids in our findings. Interestingly, in hamsters higher attacks to the belly region occur with transitions to adulthood from puberty and exposure to stressors (or glucocorticoids) accelerates the production of attacks to the region [9,43,44]. Thus, lower attacks to the ventral portion of the mid-section (including belly) of the intruder by KO mice would be consistent with lower glucorticoid activity in these mice.…”

Section: Discussionmentioning

confidence: 83%

Intermale aggression in corticotropin-releasing factor receptor 1 deficient mice

Gammie

Stevenson

2006

Behavioural Brain Research

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The anxiogenic neuropeptide, corticotropin-releasing factor (CRF), has a complex effect on intermale aggression. CRF receptor 1 (CRFR1) is the primary receptor for CRF and in this study, we examined in detail isolation-induced intermale aggression in CRFR1 deficient mice. All mice contained a mixed 50:50 inbred/outbred background to improve aggressive performance. Mice were isolated for 4 weeks prior to two consecutive days of aggression testing using the resident-intruder paradigm. Mice were also tested for anxiety on the elevated plus maze. Relative to littermate wild-type (WT) controls, CRFR1-mutant mice exhibited normal levels of intermale aggression over the two test days in terms of percentage showing aggression, number of attacks, time aggressive, and latency to first attack. In terms of sites of attacks on intruders, CRFR1-deficient mice attacked the ventral portion of the midsection (including belly) significantly less frequently than WT males on test day 1, but these differences did not reach significance on test day 2. No other differences in sites of attacks were observed. Tail rattling also did not differ between groups. Importantly, KO males showed decreased anxiety relative to WT mice (consistent with previous reports) as evidenced by spending significantly more time on the open arms and significantly less time on the closed arms of the elevated plus maze. Plus maze performance did not correlate with any measure of levels of aggression, suggesting a dissociation between altered levels of anxiety and aggressive performance. Taken together, the results suggest that the activation CRFR1 is not necessary for the normal production of isolation-induced intermale aggression.

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Section: Discussionmentioning

confidence: 83%

Intermale aggression in corticotropin-releasing factor receptor 1 deficient mice

Gammie

Stevenson

2006

Behavioural Brain Research

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“…By contrast, exposure to aggressive adults in late adolescence inhibits offensive aggression [16,70]. Another important factor is social play, a major source of social experience during the adolescent period of many mammals [71,72].…”

Section: The Shaping Of Behavioural Profiles During Adolescencementioning

confidence: 99%

Behavioural profiles are shaped by social experience: when, how and why

Sachser

Kaiser

Hennessy

2013

Phil. Trans. R. Soc. B

134

158

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The comprehensive understanding of individual variation in behavioural profiles is a current and timely topic not only in behavioural ecology, but also in biopsychological and biomedical research. This study focuses on the shaping of behavioural profiles by the social environment in mammals. We review evidence that the shaping of behavioural profiles occurs from the prenatal phase through adolescence and beyond. We focus specifically on adolescence, a sensitive phase during which environmental stimuli have distinctive effects on the modulation of behavioural profiles. We discuss causation, in particular, how behavioural profiles are shaped by social stimuli through behavioural and neuroendocrine processes. We postulate a central role for maternal hormones during the prenatal phase, for maternal behaviour during lactation and for the interaction of testosterone and stress hormones during adolescence. We refer to evolutionary history and attempt to place developmental shaping into broader evolutionary historical trends. Finally, we address survival value. We argue that the shaping of behavioural profiles by environmental stimuli from the prenatal phase through adolescence represents an effective mechanism for repeated and rapid adaptation during the lifetime. Notably, the adolescent phase may provide a last chance for correction if the future environment deviates from that predicted in earlier phases.

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“…Importantly, exposure to high rates of stress around puberty has been related to an increase of violent behaviors and personality disorders (PD) [note that a very high percentage of individuals that commit violent repeated offenses suffer PD (Putkonen et al, 2003)]; although this is typically reported in men (Wolff and Shi, 2012) evidence is also available in women (Foy et al, 2012). Animal research has shown that exposure to stressful events during puberty increases agonistic behaviors during adolescence and adulthood in several species (Delville et al, 2003;Sachser, 1993).…”

Section: Introductionmentioning

confidence: 99%

Long-term programming of enhanced aggression by peripuberty stress in female rats

Cordero

Ansermet

Sandi

2013

Psychoneuroendocrinology

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Summary Human literature has linked adverse early life experiences with an increased risk to develop violent behaviors in both boys and girls. We have previously shown that male rats submitted to stress during the peripuberty period display as adults abnormal aggressive behavior against both male intruders and female partners. In the present study, we examined whether the same stress protocol would affect the development of aggressive behaviors in female rats. We evaluated the behavior of these peripuberty stressed female rats when confronted, at adulthood, with either female or male intruders, and during their cohabitation with male partners. Given that estrus cycle influences mood and aggressive behaviors, female aggressive behavior was assessed at different estrus cycle phases: estrus and diestrus, and during pregnancy and lactancy. Additionally, we evaluated postpartum plasma levels of vasopressin, oxytocin and corticosterone, hormones associated with aggression and the regulation of social behavior. Compared to control females, females submitted to stressful events during puberty exhibited higher and more sustained rates of aggression during adulthood independently on the estrus cycle or the sex of the intruder, and they had higher levels of plasma vasopressin. Significant correlations between plasma levels of vasopressin and corticosterone and aggressive behavior were also found. Strikingly, our results showed opposite intragroup correlations suggesting a different role of these hormones on aggression depending on life experiences. We provide here an animal model, devoid of cultural influences strongly supporting a role for biological factors in the development of aggressive behaviors following exposure to stressful events at puberty in females. #

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Stress and the development of agonistic behavior in golden hamsters

Cited by 77 publications

References 59 publications

Intermale aggression in corticotropin-releasing factor receptor 1 deficient mice

Intermale aggression in corticotropin-releasing factor receptor 1 deficient mice

Behavioural profiles are shaped by social experience: when, how and why

Long-term programming of enhanced aggression by peripuberty stress in female rats

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