Program & Abstract Book - EPFL Latsis Symposium 2009

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EPFL Latsis Symposium 2009: Understanding Violence S-17 42 February 11-13 2009 ge n e t i c a n D e a r l y e n v i r o n m e n t a l f a c t o r s s h a p i n g a D u l t m a l e a g g r e s s i o n Neumann, Inga D. Department of Behavioural and Molecular Neuroendocrinology University of Regensburg, Germany Aggression constitutes a central problem in our societies and is also linked to several psychopathologies, including stress-related affective disorders. Moreover, adverse early life experiences like emotional neglect and abuse, are established risk factors not only for the development of anxiety- and depression-related disorders, but also of abnormal or excessive forms of adult aggression. However, comparable animal studies on aggression are lacking. Here, we present animal models to study the influence of the genetic background for either high (HAB) or low (LAB) anxiety-related behaviour, as well the influence of early life stress on adult intermale aggression. First, we analyzed the aggression behaviour of HAB and LAB male Wistar rats during a 10-min resident-intruder (RI) test. LAB males displayed more aggressive behaviour than HAB or non-selected NAB males, which was reflected by more attacks and a shorter attack latency, and accompanied by a more pronounced plasma ACTH response, differential neuronal activation within relevant brain regions (PVN, septum), and a decrease in lateral septal vasopressin release as measured by intracerebral microdialysis (1,2). Moreover, LAB males show abnormal aggression towards a narcotized male, and a female intruder, respectively. Moreover, we analyzed the effects of maternal separation (MS) on juvenile play-fight behaviour as well as on adult intermale aggression. Juvenile MS rats showed a significant increase in offensive play-fighting (more nape attacks and vigorous fur pulling, less supine postures), and an increase in adult aggression during the RI test (more lateral threat, keep down and offensive upright). In order to understand possible underlying neurobiological mechanisms, we quantified vasopressin mRNA expression, as the brain vasopressin system is an important modulator of complex social behaviors including aggression. Interestingly, an increased vasopressin mRNA expression was found in the PVN of juvenile and adult MS rats (3). In order to reveal genetic X environmental interaction, HAB and LAB rats were exposed to MS. Quantification of adult intermale aggression revealed differential effects of MS depending on the genetic background thus confirming recent results in the context of anxiety- and stress-related adult parameters in early life-stressed HAB and LAB rats (4,5). Thus, the use and establishment of relevant animal models will enable us to reveal the genetic and early environmental factors which shape adult male aggression and underlying neuronal mechanisms. Supported by BMBF and DFG (IDN)
EPFL Latsis Symposium 2009: Understanding Violence S-18 Abstracts for Speakers ag g r e s s i o n a n D vi o l e n c e in a n i m a l s; r o l e o f p e r s o n a l i t y f a c t o r s Koolhaas, Jaap M. Behavioral Physiology, University of Groningen, The Netherlands While most animal studies of aggression concern aggressive behavior as a functional and adaptive form of social behavior, studies in humans often focus on impulsive aggression and violence as maladaptive forms of aggressive behavior. Violence can be defined as a form of aggression that is both out of control and out of context and lacks its social communicative function. Little is known about the factors involved in the change from adaptive aggression into violence. A number of animal experiments will be discussed aimed at the interaction between individual predisposition and previous social experience in the development of violence. Our research on feral (wild-derived rodents) shows that offensive aggression is more generally related to coping with environmental challenges. Highly aggressive males adopt a proactive coping style, whereas low levels of aggression reflect a more passive or reactive coping style. These divergent coping styles have now been observed in a wide variety of species and determine adaptive capacity and vulnerability to stress related pathologies, including disorders characterized by outbursts of intense aggression and violence. Recent experiments show that the proactive coping style is characterised by a high propensity to develop violence. The underlying factor in the transition of adaptive aggression into violence seems to be the gradual reduction of inhibitory control of aggression in the course of repeated winning experience. For example, an extensive sequential analysis of the pre-attack behavior of two interacting males shows that the aggressive behavior of the proactive animal becomes more and more independent of the opponent after repeated winning. Experienced, highly aggressive males no longer respond to social signals from the opponent and develop escalated, indiscriminating and injurious forms of offensive aggression. Our animal models allow the identification of underlying physiological and neurochemical systems involved in the transition from aggression to violence. The presentation will focus on brain serotonin (5-HT) as the major orchestrator of aggression in many species including humans. However, the current view of the role of 5-HT in aggression is too simple. For example, the paradox between the serotonin deficiency hypothesis of aggression and the inhibitory effects of 5-HT on aggression clearly needs a solution. Recent studies on the 5-HT system before, during and after normal adaptive and pathological forms of aggression emphasize the importance of a clear distinction between aggression and violence. Offensive aggression, aimed at territorial control and social dominance is positively related to 5-HT neuronal activity. The violent form of aggression is associated with a tonic, trait-like reduction in 5-HT activity. Experiments in male rats and mice show that this reduction is due to an excessive serotonergic auto-inhibition predominantly mediated via an enhanced sensitivity of the somatodendritic 5-HT1A auto-receptors. Future research will address the question how this dynamic change in the tonic inhibitory control of the 5-HT neuron in the course of the development of violent trait characteristics may affect the activity of the neuron during the violent act itself. 43
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