title: Genetic selection for coping style predicts stressor susceptibility.
abstract: Genetically selected aggressive (SAL) and nonaggressive (LAL) male wild house-mice which show distinctly different coping styles, also display a differential regulation of the hypothalamic-pituitary-adrenal axis after exposure to an acute stressor. To test the hypothesis that coping style predicts stressor susceptibility, the present study examined line differences in response to a chronic stressor. Chronic psychosocial stress was evoked using two paradigms. In the first paradigm, a SAL or LAL male was living in sensory contact (except tactile contact) with a dominant SAL male for 25 days (sensory contact stress). In the second paradigm, a SAL or LAL male was, in addition to the first paradigm, defeated by a SAL male for 21 consecutive days (defeat stress). The sensory contact stressor induced in LAL mice chronic body weight loss and increased plasma adrenocorticotropic hormone levels compared to SAL mice and increased corticosterone levels, thymus involution and lower hippocampal mineralocorticoid receptor (MR) : glucocorticoid receptor (GR) ratio compared to LAL controls. The defeat stressor increased corticosterone secretion and caused adrenal hypertrophy and thymus involution in both mouse lines. Defeated LAL mice showed long-lasting body weight loss and higher corticosterone concentrations than SAL mice and lower hippocampal MR : GR ratio and decreased immobility behaviour in the forced swimming test than LAL controls. Hypothalamic corticotropin-releasing hormone mRNA expression was higher in defeated SAL than in controls. The present data show that both stress paradigms induced line-dependent physiological and neuroendocrine changes, but that the sensory contact stressor produced chronic stress symptoms in LAL mice only. This latter stress paradigm therefore seems promising to analyse the role of genetic factors in the individual differences in stress-related psychopathology.
authors.affiliation: Department of Animal Physiology, Centre for Behavioural and Cognitive Neuroscience, University of Groningen, The Netherlands. a.h.veenema@biol.rug.nl
authors.forename: A H
authors.initials: AH
authors.lastname: Veenema
authors.forename: O C
authors.initials: OC
authors.lastname: Meijer
authors.forename: E R
authors.initials: ER
authors.lastname: de Kloet
authors.forename: J M
authors.initials: JM
authors.lastname: Koolhaas
mesh_terms: D000223:Adaptation, Psychological / Q000502:physiology*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000374:Aggression / Q000502:physiology*; D000818:Animals; D001835:Body Weight; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism; D004198:Disease Susceptibility; D004291:Dominance-Subordination; D005260:Female; D006624:Hippocampus / Q000502:physiology; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D008297:Male; D018782:Maze Learning / Q000502:physiology; D051379:Mice; D012333:RNA, Messenger / Q000032:analysis; D011965:Receptors, Glucocorticoid / Q000235:genetics; D018161:Receptors, Mineralocorticoid / Q000235:genetics; D011985:Receptors, Serotonin / Q000378:metabolism; D044263:Receptors, Serotonin, 5-HT1; D013315:Stress, Psychological / Q000235:genetics*; D013550:Swimming
chemical_list: D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D018161:Receptors, Mineralocorticoid; D011985:Receptors, Serotonin; D044263:Receptors, Serotonin, 5-HT1; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone