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PubMed1993

Genetic analysis of different kinds of aggressive behavior.

Various kinds of aggressive behavior such as spontaneous intermale aggression, predatory aggression (locust-killing behavior), and irritable (shock-induced) aggression were investigated in inbred strains of mice. Genotype was shown to affect significantly the phenotypic variety of these kinds of aggression. There were, however, no interstrain correlations either between intermale aggression and predatory behavior or between intensity of intermale, shock-induced aggression and locust-killing behavior. Moreover, the intermale aggression level (percentage of fighting mice in each strain) did not correlate with the intensity of fighting. It has been shown by Mendelian analysis on C57BL/6J and BALB/c strains that these indices of intermale aggression are under different genetic control. The selection of Norway rats over 20 generations for reduced fear-induced aggressiveness toward man resulted in a decrease in irritable aggression and loss of an aggressive response to man. No changes in intermale and predatory aggression, however, were found. Hence, different kinds of aggressive behavior--intermale, predatory, and fear-induced aggression--seem to be controlled by different genetic mechanisms.

Aggression↗
PubMed2001

Zolmitriptan--a 5-HT1B/D agonist, alcohol, and aggression in mice.

RATIONALE: Zolmitriptan is an anti-migraine agent with action at 5-HT1B/D receptors. It penetrates into the central nervous system and, like other 5-HT1B/D agonists, its pharmacotherapeutic profile may include significant anti-aggressive effects. OBJECTIVES: To examine whether zolmitriptan has potential anti-aggressive effects by studying two kinds of aggressive behavior in mice--species-typical and aggression under the influence of alcohol. A second objective was to study whether pre- or post-synaptic receptors mediate these anti-aggressive effects. METHODS: Initially, the anti-aggressive effects of zolmitriptan were studied in male CFW mice during 5-min resident-intruder confrontations. To confirm the 5-HT1B receptor as a critical site of action for the anti-aggressive effects, the zolmitriptan dose-effect determinations were repeated after pretreatment with GR 127935 (10 mg/kg, i.p.). In further experiments, mice were treated concurrently with alcohol (1.0 g/kg, p.o.) and zolmitriptan (1-30 mg/kg, i.p.) in order to compare the effects of this agonist on species-typical and alcohol-heightened aggression. Finally, mice were infused with the neurotoxin 5,7-DHT (10 microg) into the raphé area to eliminate somatodendritic and presynaptic autoreceptors. The anti-aggressive effects of zolmitriptan (17 mg/kg, i.p.) or CP-94,253 (10 mg/kg, i.p.) were assessed 10 days after the lesion, and levels of 5-HT and 5-HIAA were measured in the hippocampus and prefrontal cortex. RESULTS: Zolmitriptan exerted behaviorally specific anti-aggressive effects. The reduction in aggression was antagonized by GR 127935, indicated by a rightward shift in the dose-effect curves of zolmitriptan, showing the specificity for the 5-HT1B receptors. Zolmitriptan also decreased alcohol-heightened aggression with equal efficacy. The anti-aggressive effects of CP-94,253 and zolmitriptan remained unaltered by 5,7-DHT lesions that depleted cortical and hippocampal 5-HT by 60-80%. CONCLUSIONS: Zolmitriptan proved to be an effective and behaviorally specific anti-aggressive agent in situations that engender moderate and alcohol-heightened levels of aggression. These effects are potentially due to activation of post-synaptic 5-HT1BD receptors.

Aggression↗
PubMed2005

Aggression, and some related psychological constructs (anger, hostility, and impulsivity); some comments from a research project.

The purpose of the present study was: first, to offer a few theoretical considerations on the concept of human aggression and its main types; and second, to analyse the relationship between those types of aggression and other related psychological constructs, such as anger, hostility, and impulsivity, summarizing the main empirical results of our research in progress. In order to assess their eventual correlations, several self-report techniques were compared: (a) AQ, used to measure several kinds of aggression, anger, and hostility; (b) CAMA, a questionnaire already used in a variety of cultures, for measuring attitudes toward interpersonal aggression in different instrumental and hostile situations; (c) ASQ, an instrument for measuring experienced anger and its expression in assertive or aggressive ways; and (d) BIS, used to prove three impulsiveness sub-traits: motor, attentional, and non-planning impulsiveness. The different definitions of aggression may be grouped according to whether the primary goal is distress or harm, focusing primarily on the objective infliction of harm, or on the subjective intention of harming. Most classifications in the literature show two kinds of aggression, even if different names are used: Hostile Aggression (among other names it is also known as 'reactive, impulsive, or affective') is an act primarily oriented to hurt another individual; and Instrumental Aggression (also known as 'proactive, premeditated, or predative') is a means or tool for solving problems or for obtaining a variety of objectives. As predicted, there was a positive correlation between experience and expression of anger. Anger involved physiological arousal and prepared for aggression. Anger and impulsiveness were also positively correlated with hostile aggression, but not with instrumental aggression. In the case of impulsiveness, non-planning impulsiveness was positively correlated with some situations related to hostile aggression, such as emotional agitation or lack of communication, but not with instrumental one. Finally, hostility positively correlated with anger and different kinds of aggression, but not its degree of justification. In sum, aggression can be reflected in the different personality constructs, measured by self-reports.

Aggression↗
PubMed2004

Opposing hormonal mechanisms of aggression revealed through short-lived testosterone manipulations and multiple winning experiences.

Territorial aggression is influenced by many social and environmental factors. Since aggression is a costly behavior, individuals should account for multiple factors such as population density or reproductive status before engaging in aggression. Previous work has shown that male California mice (Peromyscus californicus) respond to winning aggressive encounters by initiating aggression more quickly in future encounters, and we investigated the physiological basis for this effect. We found that injections that produced a transient increase in testosterone (T) following an aggressive encounter caused males to behave more aggressively in an encounter the following day. Experience alone was not enough to change aggression, as males treated with saline injections showed no change in aggression. The effect of T injections on aggression was androgen-based, as the inhibition of aromatase did not block the T injections from increasing aggression. Aromatase inhibition did, however, increase aggression in the initial aggression tests (before application of T or saline injections), and aromatase activity in the bed nucleus of the stria terminalis (BNST) was negatively correlated with aggression. A previous study suggested that aromatase activity in the BNST decreases after males become fathers. Thus, distinct neuroendocrine mechanisms allow male California mice to adjust aggressive behavior in response to changes in social and reproductive status.

Aggression↗
PubMed1987

Evidence for aggression-modulating pheromones in prepuberal pigs.

A series of behavioral bioassays were conducted to determine the aggression-influencing properties of urine and other fluids. Subjects were prepuberal castrated male and female domestic pigs from commercial stocks. In the behavior assay, pigs were painted with a test fluid and grouped for a videotaped 90 min observation period. Experiment 1 validated use of videotape recording by showing that duration of aggressive behavior registered live was correlated with that obtained from video records (R = .98). In experiment 2, urine and plasma collected from actively aggressive pigs reduced the durations of aggressive behavior of test pigs compared with the effects of urine and plasma collected from socially stable, handled pigs. In Experiment 3, a new set of test pigs confirmed that urine from fighting pigs reduced the duration of attack by test pigs compared with urine from nonfighting, handled pigs. In addition, the suggested reproductive pheromone, 5 alpha-androst-16-en-3-one, substantially reduced the duration of attack. The effects of gender and aggressive state of urine-donor pigs on test pigs was determined in Experiment 4. Again, urine from castrated male and female aggressive pigs reduced attack by test pigs compared with the level of attack shown by test pigs coated with urine from handled castrated males and females. Urine from fighting and nonfighting intact males had similar effects on test pig aggression. In Experiment 5, urine was obtained from nonhandled, socially stable pigs in their home pens and again from the same pigs after they had been regrouped (aggressive). These urine types had no significant influence on test pigs' aggression over the entire 90-min observation. However, during the first 30 min nonhandled, nonfighting pigs' urine induced less aggression in test pigs than did urine from fighting pigs. Results indicate that urine and blood plasma from aggressive pigs reduces aggression by test pigs compared with the effects of urine from handled pigs. Handling may increase the aggression-promoting properties of urine, and aggression may inhibit this aggression-promoting property.

Aggression↗
PubMed1976

Influence of colony lighting conditions on home-cage spontaneous aggression.

In a series of experiments the effects of colony lighting conditions on home-cage aggression were examined, and the relation among measures of home-cage aggressive behavior and shock-induced aggression were determined. In each experiment rats were maintained under either a light/dark (LD) cycle or a continous light (LL) schedule. Experiments 1A and 1B indicated that for cages of LD rats the highest rates of home-cage aggression occurred during the dark segment of the light cycle whereas the lowest rates of aggression characterized the light segment. In contrast, the rate of home-cage aggression was low and constant across time periods for cages of LL rats. Reflecting these differences between lighting conditions, regression analyses in Experiment 1B identified a periodic trend following the fundamental sine curve in the home-cage aggression data from cages of LD rats but not in the data from cages of LL rats. In Experiment 2 the relation between individual differences in home-cage aggression and shock-induced aggression and shock-induced aggression was found to be time dependent for pairs of LD rats. Correlations based on scores of home-cage aggression and shock-induced aggression obtained during the dark segment were positive and statistically significant. Correlations of these two aggressive behaviors based on scores obtained during the light segment were not statistically significant. For pairs of LL rats, no time-dependent pattern in the relation of home-cage aggression to shock-induced aggression was observed.

Aggression↗
PubMed2005

5-HT(3) receptors, alcohol and aggressive behavior in mice.

Alcohol is a positive modulator at the 5-HT(3) receptor, which has been implicated in alcohol drinking, anxiety and aggression. The reported experiments explored the role of the 5-HT(3) receptor in aggressive behavior and alcohol-heightened aggression. Male, CFW mice were trained to self-administer 1.0 g/kg of alcohol, after which they confronted an intruder. Half of the CFW mice exhibited consistently increased aggressive behavior after alcohol and were designated as showing alcohol-heightened aggression, the others showed no increase and were designated as showing alcohol non-heightened aggression. The 5-HT(3) antagonist, ondansetron (0.01-1.0 mg/kg), significantly reduced aggression in both groups of CFW mice without affecting non-aggressive behaviors. Zacopride also reduced aggression effectively in both groups of mice, but at high doses began to affect walking. Male B6SJL/F2 transgenic 5-HT(3) over-expressing mice (TG) and wild-type mice (WT) were tested for aggressive behavior in their home cage. In those individuals that fought in tests of resident-intruder aggression, no differences were found in aggression after alcohol intake. In tests of aggression without alcohol intake, zacopride reduced aggression in both TG and WT mice at a dose of 56 mg/kg. Antagonism of 5-HT(3) receptors shows promising anti-aggressive effects, although these effects depend on the genetic background of the mice.

Aggression↗
PubMed2005

Acute effects of lorazepam on laboratory measures of aggressive and escape responses of adult male parolees.

Acute benzodiazepine administrations typically decrease aggressive responding, but increases in aggression have been reported in some studies. The benzodiazepine lorazepam has been studied less frequently than other benzodiazepines in aggression research, although it is often used to suppress violent aggression in patients. The present study was designed to investigate the effects of acute administrations of lorazepam on aggressive responding in adult humans on a laboratory aggression task. Eight adult males participated in experimental sessions on the Point Subtraction Aggression Paradigm (PSAP), which provided subjects with aggressive, escape and monetary-reinforced response options. Acute oral doses (1, 2 and 4 mg) of lorazepam decreased both aggressive responding and monetary-reinforced responding in seven of eight subjects. In one subject, lorazepam produced dose-dependent increases in aggressive responding. The effects of lorazepam on escape responding were the same as the effects on aggressive responding. The results are consistent with prior research using the PSAP and clinical data showing that benzodiazepines generally decrease aggression, and contrast with other studies that have shown that benzodiazepines can increase aggression. Since lorazepam affected both aggressive and escape responding, it is suggested that while lorazepam often produces sedation, it also modifies human aggressive responding, in part, by suppressing reactions to aversive stimuli.

Adult↗
PubMed1989

Aggression between peers in early childhood: individual continuity and developmental change.

43 children were observed in play with "best available friends" at 2 and again at 5 years of age. An arousing stimulus, an angry interaction between adults, was introduced during play sessions to increase the likelihood of elicitation of aggressive patterns. Dimensions of physical aggression at age 2 (e.g., object-related aggression, bodily aggression) predicted dimensions of children's physical aggression at age 5. However, substantial sex differences in the stability of aggression were found. Among boys, the disposition to engage in physical aggression was highly stable, with correlations ranging as high as r = .76. Certain dimensions of physical aggression at age 2 were also positively associated with verbal aggression at age 5. Fewer and more modest correlations were found among girls. The frequency of aggression, particularly bodily aggression (e.g., hitting, pushing), initiations of aggression, and the average length of aggression episodes, decreased between 2 and 5 years of age. These results indicate that relative aggressiveness tends to remain stable despite declines in the frequency of aggressive behavior between 2 and 5 years of age.

Aggression↗
PubMed2001

Developmental trajectories of physical aggression from school entry to late adolescence.

The developmental perspective applied to psychopathology has led to the concept of early- and late-onset disorders. This study explores the application of the early- and late-onset concepts of antisocial behavior to physical aggression. Are there two categories of chronically physically violent adolescents: those who are physically aggressive throughout childhood and those who start being physically aggressive during adolescence? The estimation of developmental trajectories for repeated measures of two different response variables physical aggression in childhood as measured by teacher reports and physical aggression in adolescence as measured by self-reported violent delinquency is achieved with a semi-parametric, group-based method. This new method is applied to a large sample of males from Montreal who have been assessed repeatedly since kindergarten. Several salient findings emerge from the analysis. First, we find considerable change in the levels of childhood and adolescent physical aggression. Thus, there is little evidence of stability of behavior in an absolute sense. A second key finding concerns the connection of childhood aggression to adolescent aggression. Boys with higher childhood physical aggression trajectories are far more likely to transition to a higher-level adolescent aggression trajectory than boys from lower childhood physical aggression trajectories. However, for all childhood physical aggression trajectory levels the modal transition is to a relatively low-level adolescent aggression trajectory. Third, we find little evidence of "late onset" of high-level physical aggression. Specifically, the joint trajectory analysis finds no evidence of transition from a low physical aggression trajectory in childhood to a high trajectory in adolescence.

Adolescent↗
PubMed2000

Maternal aggression in endothelial nitric oxide synthase-deficient mice.

Lactating female rodents protect their pups by expressing fierce aggression, termed maternal aggression, toward intruders. Mice lacking the neuronal nitric oxide synthase gene (nNOS-/-) exhibit significantly impaired maternal aggression, but increased male aggression, suggesting that nitric oxide (NO) produced by nNOS has opposite actions in maternal and male aggression. In contrast, mice lacking the endothelial nitric oxide synthase gene (eNOS-/-) exhibit almost no male aggression, suggesting that NO produced by eNOS facilitates male aggression. In the present study, maternal aggression in eNOS-/- mice was examined and found to be normal relative to wild-type (WT) mice in terms of the percentage displaying aggression, the average number of attacks against a male intruder, and the total amount of time spent attacking the male intruder. The eNOS-/- females also displayed normal pup retrieval behavior. Because a significant elevation of citrulline, an indirect marker of NO synthesis, occurs in neurons of the hypothalamus of lactating WT mice in association with maternal aggression, we examined the brains of eNOS-/- females for citrulline immunoreactivity following an aggressive encounter. The aggressive eNOS-/- females exhibited a significant elevation of citrulline in the medial preoptic nucleus and the subparaventricular zone of the hypothalamus relative to unstimulated lactating eNOS-/- females. Taken together, these results suggest that NO produced by eNOS neither facilitates nor inhibits maternal aggression and that NO produced by eNOS has a different role in maternal and male aggression.

Aggression↗
PubMed2002

Relationships between hormones and aggressive behavior in green anole lizards: an analysis using structural equation modeling.

We investigated the relationship between aggressive behavior and circulating androgens in the context of agonistic social interaction and examined the effect of this interaction on the androgen-aggression relationship in response to a subsequent social challenge in male Anolis carolinensis lizards. Individuals comprising an aggressive encounter group were exposed to an aggressive conspecific male for 10 min per day during a 5-day encounter period, while controls were exposed to a neutral stimulus for the same period. On the sixth day, their responses to an intruder test were observed. At intervals, individuals were sacrificed to monitor plasma androgen levels. Structural equation modeling (SEM) was used to test three a priori interaction models of the relationship between social stimulus, aggressive behavior, and androgen. Model 1 posits that exposure to a social stimulus influences androgen and aggressive behavior independently. In Model 2, a social stimulus triggers aggressive behavior, which in turn increases circulating levels of androgen. In Model 3, exposure to a social stimulus influences circulating androgen levels, which in turn triggers aggressive behavior. During the 5 days of the encounter period, circulating testosterone (T) levels of the aggressive encounter group followed the same pattern as their aggressive behavioral responses, while the control group did not show significant changes in their aggressive behavior or T level. Our SEM results supported Model 2. A means analysis showed that during the intruder test, animals with 5 days of aggressive encounters showed more aggressive responses than did control animals, while their circulating androgen levels did not differ. This further supports Model 2, suggesting that an animal's own aggressive behavior may trigger increases in levels of plasma androgen.

Aggression↗
PubMedDate not supplied

Role of dopamine receptors in the regulation of aggression in mice; relationship to genotype.

The interline differences in the manifestation of aggression evoked by stimulation was studied in mice of eight inbred lines, and the role of different types of dopamine (DA) receptors in its manifestation was investigated. Aggression was assessed in a test involving the effect of a weak electrical stimulation through the floor of the cage. A significant relationship to the animals' genotype was demonstrated, and low-aggression (C3h/He, DD, BALB/c, and AKR) and high-aggression (CBA, DBA/2, and CC57Br) lines could be distinguished on the basis of the level of aggressivity. The mixed agonist of DA receptors, apomorphine, in a one-time administration activated aggressivity in the low-aggression mice. The selective stimulation of D2-receptors with bromocriptine substantially increased the evoked aggressivity in the low-aggression mice; the blockade of D2-receptors by sulpiride decreased or prevented the manifestation of aggressivity in the high-aggression lines. At the same time, the selective D1-agonist SKF 38393 and the selective D1-antagonist SCH 23390 did not exert a substantial influence on evoked aggressivity. Evidently the D2-receptors play a key role in the control of aggression evoked by stimulation, which constitutes a model of affective aggression.

Aggression↗
PubMed1992

Alcohol and "bursts" of aggressive behavior: ethological analysis of individual differences in rats.

A quantitative ethological analysis of rodent aggression was performed in order to characterize the aggression-heightening effects of alcohol in certain individuals. In dyadic confrontations, a resident rat pursues, threatens and attacks an intruder, who reacts with defensive, flight and submissive behaviors. The behavioral data from five series of experiments conducted from 1984 through 1989 were subjected to a lag sequential analysis that identified highly predictable sequences of aggressive behavior, and to interval analysis that delineated a burst pattern of aggressive behavior. These analyses revealed a distinct behavioral sequence of pursuit----sideways threat----attack bite----aggressive posture that occurs in bursts with an inter-event interval of less than 6.6 s. In the total population, alcohol heightened attack behavior at low acute doses (0.1, 0.3, 1.0 g/kg) in 47% of the animals (n = 44), suppressed reliably attack behavior in another 25% (0.1-3.0 g/kg; n = 23) and had unreliable effects in the remaining 28% (n = 24). The peak enhancement of aggressive behavior was seen over more than a log cycle of alcohol doses (0.1, 0.3 or 1.0 g/kg) in different individuals. In an additional group of rats (n = 20), individuals were identified according to whether or not acute low alcohol doses enhanced or suppressed the frequency of attack bites. In the subgroup of five rats who doubled their attack frequency upon acute alcohol challenge, this aggression-heightening effect was confirmed on repeated occasions. The aggression-heightening effects of alcohol were seen during the high-rate interactions in the initial phase of the confrontation and particularly during the lower level of fighting later on. Regardless of alcohol dose and subgroup, the highly predictable sequence of pursuit----sideways threat----attack bite----aggressive posture remained intact as long as the individual was able to fight. The present analysis identifies those individuals in whom low alcohol doses increase the frequency of attack behavior, the number of aggressive elements in bursts and particularly the "time in burst". Alcohol produces these changes without altering the latency to initiate aggressive behavior, the rate of aggressive behavior within a burst or the number of bursts in an encounter. Alcohol may lengthen aggressive bursts by preventing termination of longer aggressive sequences rather than by altering the initiation of this behavior.

Aggression↗
PubMed1992

Increased GABAA-dependent chloride uptake in mice selectively bred for low aggressive behavior.

Selective breeding for aggressive behavior alters GABA-dependent chloride uptake and behavioral response to benzodiazepine treatment. Pharmacological and biochemical studies examined subjects from three lines of adult male ICR mice selectively bred for either high levels or low levels of aggressive behavior, as well as unselected controls. Selective breeding produced two lines of behaviorally distinct males. During 5-min dyadic confrontations with an outbred stimulus animal, untreated low-aggressive mice spent more time in walking, rearing, and social interaction than untreated high-aggressive mice. The three lines also showed different responsiveness to the aggression increasing and decreasing effects as well as the sedative effects of benzodiazepine treatment. High doses of chlordiazepoxide (17, 30 mg/kg) reduced motor behaviors (walk, rear and groom) in the low-aggressive line without altering these behaviors in the high aggressive line. In the high-aggressive line, the same doses of chlordiazepoxide (17, 30 mg/kg) produced a behavioral shift; aggressive behaviors were reduced while social behaviors increased to levels similar to the untreated low-aggressive line. In contrast, only the unselected line pursued and threatened more after a low dose of chlordiazepoxide (3 mg/kg). The three lines also showed alterations at the GABAA-benzodiazepine receptor complex. Specific uptake of [3H]Ro-15-1788 was increased in cerebral cortex, hypothalamus and hippocampus in the low-aggressive line, and was reduced in these areas in high-aggressive line when compared with unselected controls. Similarly, GABA-dependent chloride uptake in cortical synaptoneurosomes was augmented in low-aggressive mice and decreased in high-aggressive mice when compared to unselected controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Aggression↗
PubMed1995

-Fos expression in female hamster brain following sexual and aggressive behaviors.

The goal of these experiments was to use c-Fos immunocytochemistry to determine areas of the female hamster brain that are active during lordosis and aggression. Ovariectomized hamsters were given (i) estradiol and progesterone, plus a lordosis test, (ii) estradiol and progesterone, but no lordosis test, (iii) oil, plus an aggressive behavior test, or (iv) oil, but no behavior test. Results showed that following lordosis, there was increased c-Fos expression in the medial bed nucleus of the stria terminalis, medial accumbens, medial preoptic nucleus, paraventricular nucleus and medial amygdala. Following a single aggression test, c-Fos was significantly increased only within the medial amygdala. There was no effect of lordosis or aggression on c-Fos expression within the lateral or central ventromedial hypothalamus, suprachiasmatic nucleus or dorsal midbrain central gray. In a second experiment, ovariectomized female hamsters were given (i) repeated aggressive experience, (ii) a single aggression test or (iii) no aggression test. Because some females were not aggressive towards males, they became a separate group post hoc. The number of cells expressing c-Fos was higher in the medial preoptic nucleus and medial amygdala of females given a single aggressive test and in non-aggressive females vs control females. Females given prior aggressive experience showed higher c-Fos expression only in the medial preoptic nucleus. These results demonstrate that increased neural activation in several forebrain nuclei is seen after sexual or aggressive behaviors in female hamsters. However, because the pattern of c-Fos staining in the non-aggressive females was similar to the pattern in aggressive females, this questions previous conclusions regarding the behavioral specificity of these effects and suggests instead that such activation is common to social interactions in general.

Aggression↗
PubMed2005

Mechanisms differentiating normal from abnormal aggression: glucocorticoids and serotonin.

Psychopathology-associated human aggression types are induced by a variety of conditions, are behaviorally variable, and show a differential pharmacological responsiveness. Thus, there are several types of abnormal human aggression. This diversity was not reflected by conventional laboratory approaches that focused on the quantitative aspects of aggressive behavior. Recently, several laboratory models of abnormal aggression were proposed, which mainly model hyperarousal-driven aggressiveness (characteristic to intermittent explosive disorder, post-traumatic stress disorder, depression, chronic burnout, etc.) and hypoarousal-driven aggressiveness (characteristic mainly to antisocial personality disorder and its childhood antecedent conduct disorder). Findings obtained with these models suggest that hyperarousal-driven aggressiveness has at its roots an excessive acute glucocorticoid stress response (and probably an exaggerated response of other stress-related systems), whereas chronic hypoarousal-associated aggressiveness is due to glucocorticoid deficits that affect brain function on the long term. In hypoarousal-driven aggressiveness, serotonergic neurotransmission appears to lose its impact on aggression (which it has in normal aggression), certain prefrontal neurons are weakly activated, whereas the central amygdala (no, or weakly involved in the control of normal aggression) acquires important roles. We suggest that the specific study of abnormal aspects of aggressive behavior would lead to important developments in understanding the specific mechanisms underlying different forms of aggression, and may ultimately lead to the development of better treatment approaches.

Aggression↗
PubMed2006

Normal and abnormal aggression: human disorders and novel laboratory models.

We review here aggression-related human psychopathologies and propose that human aggressiveness is mainly due to three major factors: (i) brain dysfunction affecting aggression-controlling brain centers (e.g. in certain types of brain lesions, epilepsy, Alzheimer disease, etc.); (ii) hypoarousal associated with chronically low plasma glucocorticoids, which foster violence by diminishing emotional barriers that limit such behaviors (e.g. in conduct disorder and antisocial personality disorder); (iii) hyperarousal which leads to irritability and outbursts (e.g. in depression, intermittent explosive disorder, chronic fatigue, etc.). Different disorders are associated with different types of aggressiveness; e.g. hypoarousal is often associated with instrumental aggression, whereas hyperarousal is associated with uncontrollable outbursts. Many psychological disorders have been simulated in laboratory models, which were used to assess aggressiveness. Little effort was invested, however, in assessing the abnormal dimension of such aggressiveness. We present here three models that appear especially suitable to assess abnormal aspects of rodent aggression: (i) abnormal attack targeting (head, throat, and belly) that is induced by hypoarousal in rats and models violence in hypoarousal-driven human aggression (ii) 'escalated' aggression (increased aggressive response due to frustration or instigation), which models irritability and hyperarousal-driven aggressiveness; and (iii) context-independent attacks induced by hypothalamic stimulation or genetic manipulations. These three models address different aspects of abnormal aggressiveness, and can become extremely useful in three areas: in evaluating and assessing models of human psychopathologies, in studying transgenic animals, and in developing new treatment strategies. Research based on these or similar models do not address aggressiveness in quantitative terms, but follows the development of abnormal aspects, and the possibilities of their specific treatment.

Aggression↗