Here is a brief summary from the article on the hypothalamic-pituitary-adrenal axis (HPA) that is associated with both anxiety and aggression through its mediation of adrenal hormones.Aggression and anxiety: social context and neurobiological linksCopyright: © 2010 Neumann, Veenema and Beiderbeck. This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.Psychopathologies such as anxiety- and depression-related disorders are often characterized by impaired social behaviours including excessive aggression and violence. Excessive aggression and violence likely develop as a consequence of generally disturbed emotional regulation, such as abnormally high or low levels of anxiety. This suggests an overlap between brain circuitries and neurochemical systems regulating aggression and anxiety. In this review, we will discuss different forms of male aggression, rodent models of excessive aggression, and neurobiological mechanisms underlying male aggression in the context of anxiety. We will summarize our attempts to establish an animal model of high and abnormal aggression using rats selected for high (HAB) versus low (LAB) anxiety-related behaviour. Briefly, male LAB rats and, to a lesser extent, male HAB rats show high and abnormal forms of aggression compared with non-selected (NAB) rats, making them a suitable animal model for studying excessive aggression in the context of extremes in innate anxiety. In addition, we will discuss differences in the activity of the hypothalamic-pituitary-adrenal axis, brain arginine vasopressin, and the serotonin systems, among others, which contribute to the distinct behavioural phenotypes related to aggression and anxiety. Further investigation of the neurobiological systems in animals with distinct anxiety phenotypes might provide valuable information about the link between excessive aggression and disturbed emotional regulation, which is essential for understanding the social and emotional deficits that are characteristic of many human psychiatric disorders.
Barbara Vollmayr, University of Heidelberg, Germany
Geert De Vries , University of Massachusetts Amherst, USA
Miriam Schneider, Central Institute of Mental Health, Germany
*Correspondence: Inga D. Neumann, Department of Behavioural and Molecular Neuroendocrinology, University of Regensburg, Universitaetsstrasse 31, 93053 Regensburg, Germany. e-mail: firstname.lastname@example.org
The HPA axis is one of the major stress systems and is regulated by the release of corticotropin-releasing hormone and AVP from the paraventricular nucleus (PVN) into the pituitary, which stimulates the secretion of ACTH into the blood. ACTH, in turn, triggers the adrenal release of glucocorticoids (cortisol in humans, corticosterone in rats), which facilitate physiological and behavioural adaptations to a stressor at multiple peripheral and brain levels. Dysregulation of the HPA axis has been frequently linked to anxiety- and depression-related disorders, as well as to violence and abnormal aggression (Plotsky et al., 1998; Mello et al., 2003; de Kloet et al., 2005). Although data from preclinical studies are conflicting, they generally implicate glucocorticoids as important regulators of aggressive behaviour (Haller et al., 1998, 2001; Summers et al., 2005b). Paradoxically, both acute high and chronically low levels of circulating glucocorticoids have been associated with high aggression (see above; Hayden-Hixson and Ferris, 1991; Haller et al., 2000; Kruk et al., 2004; Summers and Winberg, 2006). For example, an acute rise in glucocorticoids promotes intermale aggression in rodents (Mikics et al., 2004) and might be associated with a state of hyperarousal and sudden outbursts of aggression. Acute blockade of glucocorticoid synthesis results in reduced aggression in male rats, an effect which is reversible by corticosterone treatment (Mikics et al., 2004). In contrast to these findings, low HPA axis reactivity (Veenema et al., 2003b, 2005) or chronically low glucocorticoid levels (Haller et al., 2001, 2005; Kim and Haller, 2007) also result in excessive aggression and a higher frequency of attacks directed towards vulnerable body parts and might underlie pathological forms of aggression including violence.Yep, geeky stuff. But interesting for those of us who are interested in such things. OK, one more brief quote from the article that illustrates why we want to know more about this:
Two main forms of human excessive/violent aggression are described, namely impulsive-reactive-hostile-affective aggression and controlled-proactive-instrumental-predatory aggression (Vitiello and Stoff, 1997). Whereas the first form of aggression is seen in patients with depression, PTSD, or intermittent explosive disorder, the second type of aggression can be revealed in patients with personality disorders (conduct, antisocial, and borderline disorder), but may also be found in individuals without noticeable emotional or social deficits (i.e. the “friendly neighbour” or the “polite and quiet young man”). In particular, cases of violent and criminal behaviour displayed by these “unlikely” individuals are difficult to understand and indicate the urgent necessity to reveal underlying neurobiological mechanisms of abnormal aggression in more detail. Both forms of excessive aggression are associated with distinct disturbances in the regulation of emotions and alterations in autonomic and neuroendocrine functioning. More specifically, impulsive-reactive-hostile-affective aggression is generally associated with high emotional reactions and autonomic responses including high glucocorticoid levels, whereas controlled-proactive-instrumental-predatory aggression is generally associated with low emotional, autonomic, and glucocorticoid responses, and low skin conductance (summarized in Haller and Kruk, 2006). We hypothesize that the emotional responses underlying the two distinct forms of aggression are linked to differences in anxiety-mediating brain pathways.Those of us who are therapists, or are training to be therapists, will see a lot of PTSD clients, victims of violence, and we'll also see people with personality disorders, so understand how the anxiety/aggression impulses are connected in the brain can help us better serve our clients.
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