162 research outputs found

    Effect of different agonistic experiences on behavioural seizures in fully amygdala kindled rats

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    Fully amygdala kindled rats were exposed to two different inter-male agonistic experiences in order to study the interaction between epilepsy and acute social stress. Victory experience did not influence the severity of seizure behaviour, whereas a single acute defeat modified both ictal and postictal seizure manifestations. Defeat resulted in less severe and shorter lasting motor seizures, and the accompanied postictal inhibition or behavioural depression was of shorter duration in comparison with pre-stress values. The ability of acute defeat to trigger anticonvulsant activity as implied by the weakened convulsive response is discussed.

    Individual strategies of aggressive and non-aggressive male mice in encounters with trained aggressive residents

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    To determine whether individual differences in offensive behaviour are related to differences in defensive behaviour, the responses of male wild house mice, Mus domesticus, of an aggressive and a non-aggressive line to defeat by physically stronger residents were analysed. Individuals of the aggressive line engaged in more flight behaviour, whereas the males of the non-aggressive line predominantly showed immobility. The higher flight tendency of the aggressive intruders provoked more attacks by the resident, resulting in more fighting between the resident and an aggressive male than between the resident and a non-aggressive intruder. However, if offered an opportunity to escape from the home-cage of the resident, aggressive males more readily made use of it than non-aggressive intruders. Differences between aggressive and non-aggressive male mice are interpreted in terms of fundamentally different behavioural strategies adopted in response to social interaction. The response of aggressive males can be characterized as an active behavioural strategy by which they tend to determine actively their social situation. In contrast, the prevailing lack of overt attempts to manipulate the situation by the non-aggressive mice points to passive confrontation, in an offensive as well as in a defensive context.

    Coping styles and aggression:A biobehavioral approach

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    Immunity in barren and enriched housed pigs differing in baseline cortisol concentration

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    It was shown recently that barren housed pigs (small pens, no substrate) have a blunted circadian rhythm of salivary cortisol as compared to enriched housed pigs (large pens with daily fresh bedding). In the light period, enriched housed pigs showed significantly higher concentrations of cortisol in saliva than barren housed pigs, whereas in the dark period, cortisol concentrations were low in both enriched and barren housed pigs. In the present study, the immunological consequences of the difference in baseline salivary cortisol concentration in the light period were evaluated. It appeared that leukocyte and lymphocyte distributions, and in vitro lymphocyte proliferation following ConcanavalineA (ConA) stimulation in the assay using purified lymphocytes were not affected. However, barren and enriched housed pigs did show a different proliferation response to ConA in the whole blood assay. At day 2 of culture, proliferation was higher in barren housed pigs than in enriched housed pigs, whereas at day 4 of culture, proliferation was higher in enriched housed pigs than in barren housed pigs. Lymphocyte proliferation at day 2 of culture in the whole blood assay correlated negatively with plasma cortisol levels, which might thus explain the higher proliferation in barren housed pigs at day 2 of culture. The in vivo humoral and cellular (delayed type hypersensitivity, DTH) immune response to KLH was not affected by housing conditions. We conclude that, although baseline salivary cortisol concentrations differ between enriched and barren housed pigs, immune function appears to be relatively unaffected.

    Behavioral Profiles of Genetically Selected Aggressive and Nonaggressive Male Wild House Mice in Two Anxiety Tests

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    Artificially selected aggressive (SAL) and non-aggressive (LAL) male house mice were tested in a hexagonal tunnel maze and light–dark preference (LD) box to determine if the bidirectional selection for aggressive behavior leads to a coselection for different levels of trait anxiety. The tunnel maze consists of an open, brightly lit central arena surrounded by a complex system of interconnecting tunnels. As in the LD box, animals which spend less time and are less active in the brightly illuminated section of the maze are considered to have higher anxiety levels. In the tunnel maze, the LAL mice showed more exploration and spent more time in the central arena than the SAL animals, but only during the final 2 min of the 6-min test. This reduced preference for the central arena was not due to general inactivity or a failure of the SAL to find the central arena and indicates a higher level of state anxiety in the aggressive animals. In contrast, no “anxiety-like” differences were found in the LD box, either for the percentage of time spent in the light compartment or for the number of crossings. SAL males actually showed higher levels of moving and rearing, and lower levels of freezing, than did LAL males.

    Differential Effects of Neonatal Testosterone Treatment on Aggression in Two Selection Lines of Mice

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    Selection lines of mice, artificially selected for aggression based upon the attack latency score (ALS), were used. In order to determine the relative contribution of neonatal testosterone (T) in the development of aggression, we vary the plasma-T level in males of both selection lines on the day of birth. At 14 weeks the ALS was measured. Neonatal T treatment results in a reduction of aggression in the long attack latency (LAL) line, whereas aggressive behaviour of the short attack latency (SAL) line is not affected. Both selection lines show reduction in testicular weight, although the total amount of T-producing Leydig cells was not affected. Neonatal T may cause a permanent reduction in aggressive behaviour in the LAL line only, probably due to differential appearance of critical periods. It is suggested that the difference in aggressive behaviour between SAL and LAL selection lines is due to a prenatally determined difference in neonatal T sensitivity of the brain.

    Does the current concept of stress explain PTSD

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    Understanding the etiology of stress-related diseases such as PTSD requires a more fundamental understanding of stress. Since individuals may differ strongly in their response to a stressor, it is argued that stress includes not only the stimulus and the response but also the individual appraisal of the situation. This chapter discusses the stress concept, how it has evolved in the course of time, and some important components of the appraisal process. In addition to the factors controllability and predictability, outcome expectancy and feedback of the victim’s own actions during the traumatic event are suggested to be important factors in the development of stress-related disease. Preliminary preclinical studies suggest that individual differences in the way in which these factors are used in the appraisal of everyday life situations may explain individual vulnerability

    Temporal and spatial dynamics of corticosteroid receptor down-regulation in rat brain following social defeat

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    The experiments explored the nature and time course of changes in glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) binding in homogenates of various brain regions and pituitary of male Wistar rats following social defeat stress. One week after defeat, the binding capacity of GRs was decreased in the hippocampus and the hypothalamus while no changes were observed in the parietal cortex and the pituitary. The number of MRs remained at the same level as in undefeated rats. Three weeks postdefeat, the initially down-regulated GR returned to baseline level in the hippocampus and the hypothalamus. However, GR binding was now decreased in the parietal cortex. Severe down-regulation of MRs was detected in the hippocampal and septal tissue. The results show that brief but intense stress like social defeat induces a long-lasting down-regulation of corticosteroid receptors and that the temporal dynamics of these changes are not only differential for GRs and MRs but also for brain sites.

    The Vicious Cycle Towards Violence: Focus on the Negative Feedback Mechanisms of Brain Serotonin Neurotransmission

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    Violence can be defined as a form of escalated aggressive behavior that is expressed out of context and out of inhibitory control, and apparently has lost its adaptive function in social communication. Little is known about the social and environmental factors as well as the underlying neurobiological mechanisms involved in the shift of normal adaptive aggression into violence. In an effort to model the harmful acts of aggression and violence in humans, we recently (re)developed an animal model that is focused on engendering uncontrolled forms of maladaptive aggressive behavior in laboratory-bred feral rats and mice. We show that certain (8–12%) constitutionally aggressive individuals gradually develop, over the course of repetitive exposures to victorious social conflicts, escalated (short-latency, high-frequency and ferocious attacks), persistent (lack of attack inhibition by defeat/submission signals and perseverance of the aggressive attack-biting bout), indiscriminating (attacking female and anesthetized male intruders) and injurious (enhanced vulnerable-body region attacks and inflicted wounding) forms of offensive aggression. Based on the neurobiological results obtained using this model, a revised view is presented on the key role of central serotonergic (auto)regulatory mechanisms in this transition of normal aggression into violence

    Development of violence in mice through repeated victory along with changes in prefrontal cortex neurochemistry

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    Recent reviews on the validity of rodent aggression models for human violence have addressed the dimension of pathological, maladaptive, violent forms of aggression in male rodent aggressive behaviour. Among the neurobiological mechanisms proposed for the regulation of aggressive behaviour in its normal and pathological forms, serotonin plays a major role. However, the results on the detailed mechanism are still confusing and controversial, mainly because of difficulties in extrapolating from rodent to human psychopathological behaviour. Our aim was to investigate the involvement of serotonin in pathological aggression. We subjected mice genetically selected for high (SAL, TA, NC900 lines) and low (LAL, TNA, NC100) aggression levels to a repeated resident-intruder experience (RRI mice) or to handling as a control procedure (CTR mice). Pathological aggression parameters we recorded were aggression towards females and lack of communication between the resident and its opponent. In the same mice, we measured the monoamine levels in the prefrontal cortex, a brain region strongly involved in the regulation of motivated behaviour. Our results show that SAL mice augmented their proneness to attack and showed the most pathological phenotype, with disregard of the opponent's sex, high territorial behavioural patterns, and low sensitivity to signals of subordination. In contrast, TA and NC900 augmented their proneness to attack and low discrimination of the opponent's signals, without showing offence towards females. After repeated resident-intruder experience, serotonin levels in the prefrontal cortex were significantly lower in SAL than in LAL whereas dopamine turnover was significantly higher, compared to CTR mice. Serotonin turnover was significantly reduced in all RRI mice, with no strain differences. Noradrenaline was significantly lower in aggressive mice of the TA and NC900 lines compared to their low-aggressive counterparts, with no effect of the repeated resident-intruder experience. We conclude that social experience changes prefrontal cortex neurochemistry and elicits pathologically aggressive phenotypes. (C) 2008 Elsevier B.V. All rights reserved
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