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Sluyter, Frans; Arseneault, Louise; Moffitt, Terrie E.; Veenema, Alexa H.; Boer, Sietse de; Koolhaas, Jaap M.

doi:10.1023/a:1025730901955

Cited by 49 publications

(13 citation statements)

References 81 publications

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“…To understand maladaptive or pathological levels of aggression, which translates to clinically significant levels of aggression (or violence) in humans, we need to dissect those escalated types of aggression from species-typical behaviors in animal models (Miczek et al 2002, 2004; Haller and Kruk 2006; Nelson and Trainor 2007; de Boer et al, 2009). One important aspect is the nature of the attack behaviors, which can be examined by assessing the targets of attacks (Haller et al 2002) or females (Sluyter et al 2003). For example, optogenetic activation of a subdivision of the ventromedial hypothalamus (VMHvl) induced abnormal attack behavior toward females and even toward inanimate objects (Lin et al 2011).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast to the ritualistic species-typical aggressive behaviors, some models for abnormal aggression showed attacks directed at vulnerable body targets such as the face and abdominal areas (Haller et al 2001). Other models of abnormal aggression in male rodents highlight aggressive behaviors against females (Sluyter et al 2003). The form of the aggressive behaviors must be considered when evaluating whether aggression is to be considered species-typical or “pathological.”…”

Section: Introductionmentioning

confidence: 99%

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Behavioral characterization of escalated aggression induced by GABAB receptor activation in the dorsal raphe nucleus

et al. 2012

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Rationale Pharmacological activation of GABAB receptors in the dorsal raphé nucleus (DRN) can escalate territorial aggression in male mice. Objectives We characterized this escalated aggression in terms of its behavioral and environmental determinants. Methods Aggressive behavior of resident male (CFW or ICR mouse) was assessed in confrontations with a group-housed intruder. Either baclofen (0.06 nmol/0.2 μl) or vehicle (saline) was microinjected into the DRN ten minutes before the confrontation. We examined baclofen-heightened aggression in five situations: aggression in a neutral arena and after social instigation (experiment 1), aggression during the light phase of the cycle (experiment 2), aggression without prior fighting experience (experiment 3), aggression toward a female (experiment 4), and aggression after defeat experiences (experiment 5). In addition, we examined the body targets towards which bites are directed and the duration of aggressive bursts after baclofen treatment. Results Regardless of the past social experience, baclofen escalated aggressive behaviors. Even in the neutral arena and after defeat experiences, where aggressive behaviors were inhibited, baclofen significantly increased aggression. Baclofen increased attack bites directed at vulnerable body areas of male intruders but not toward a female and only in the dark. Also, baclofen prolonged the duration of aggressive bursts. Conclusions For baclofen to escalate aggression, specific stimulation (male intruder) and tonic level of serotonin (dark cycle) are required. Once aggressive behavior is triggered, intra-DRN baclofen escalates the level of aggression to abnormal levels and renders it difficult to terminate. Also, baclofen counteracts the effects of novelty or past experiences of defeat.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Behavioral characterization of escalated aggression induced by GABAB receptor activation in the dorsal raphe nucleus

et al. 2012

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“…Starting 50 years ago, three major independent selection experiments were conducted, resulting in three different strains of high- and low-aggressive mice (Miczek et al 2001): (1) the Turku Aggressive (TA) and Turku Non Aggressive (TNA) lines originated from an outbred colony of Swiss albino laboratory mice (Lagerspetz 1964; Nyberg et al 2004), (2) the aggressive Short Attack Latency (SAL) and low-aggressive Long Attack Latency (LAL) mice originated from a population of wild-trapped feral house mice (Sluyter et al 2003; van Oortmerssen and Bakker 1981) and (3) the high-aggressive NC900 and low-aggressive NC100 mice derived from an ICR (Institute of Cancer Research) laboratory Swiss-Webster outbred stock (Cairns et al 1983). Although these lines came from different genetic backgrounds and different laboratories with their own housing idiosyncrasies, and although selection criteria differed in terms of testing environment, type of test, type of opponent, the offensive aggression levels of these strains are generally comparable.…”

Section: Escalated Aggressive Behavior In Unselected Feral Animalsmentioning

confidence: 99%

Excessive aggression as model of violence: a critical evaluation of current preclinical methods

2013

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Rationale Preclinical experimental models of pathological aggressive behavior are a sorely understudied and difficult research area. Objectives How valid, reliable, productive and informative are the most frequently used animal models of excessive aggressive behavior? Methods The rationale, key methodological features, supporting data and arguments as well as their disadvantages and limitations of the most frequently used animal models for excessive aggressive behavior are summarized and their validity and reliability are evaluated. Results Excessive aggressive behavior is validly and reliably seen in (1) a proportion of feral-derived rats and selectively bred mice, (2) rats with compromised adrenal function resulting in a hypoglucocorticoid state, (3) a significant minority of mice, rats and monkeys after consumption of a moderate dose of alcohol, and (4) resident animals of various species after social instigation. Limitations of these procedures include restrictive animal research regulations, the requirement of expertise in surgical, pharmacological and behavioral techniques, and the behaviorally impoverished mouse strains that are used in molecular genetics research. Promising recent initiatives for novel experimental models include aggressive behaviors that are evoked by optogenetic stimulation and induced by the manipulation of early social experiences such as isolation rearing or social stress. Conclusions One of the most significant challenges for animal models of excessive, potentially abnormal aggressive behavior is the characterization of distinctive neurobiological mechanisms that differ from those governing species-typical aggressive behavior. Identifying novel targets for effective intervention requires increased understanding of the distinctive molecular, cellular and circuit mechanisms for each type of abnormal aggressive behavior.

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“…Several lines of mice have been selected for differences in attack latency, including the SAL and LAL mice (van Oortmerssen and Bakker, 1981), the Turku aggressive and non-aggressive mice (Sandnabba, 1996), and the North Carolina 900 and 100 mice (Gariepy et al, 1996). Among these selection lines, the SAL mice show the most excessive and abnormal forms of aggression (Sluyter et al, 2003; Haller and Kruk, 2006; Natarajan et al, 2009). However, a significant difference in anxiety-related behaviours between SAL and LAL mice has not been consistently found (Hogg et al, 2000; Veenema et al, 2003a).…”

Section: Rodent Models Of Aggression: Link To Anxietymentioning

confidence: 99%

Aggression and anxiety: social context and neurobiological links

Neumann

Veenema

Beiderbeck

2010

Front. Behav. Neurosci.

144

148

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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) vs. 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.

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Cited by 49 publications

References 81 publications

Behavioral characterization of escalated aggression induced by GABAB receptor activation in the dorsal raphe nucleus

Behavioral characterization of escalated aggression induced by GABAB receptor activation in the dorsal raphe nucleus

Excessive aggression as model of violence: a critical evaluation of current preclinical methods

Aggression and anxiety: social context and neurobiological links

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