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PubMed1993

Aggression in humans: what is its biological foundation?

Although human aggression is frequently inferred to parallel aggression based on testosterone in nonprimate mammals, there is little concrete support for this position. High- and low-aggression individuals do not consistently differ in serum testosterone. Aggression does not change at puberty when testosterone levels increase. Aggression does not increase in hypogonadal males (or females) when exogenous testosterone is administered to support sexual activity. Similarly, there are no reports that aggression increases in hirsute females even though testosterone levels may rise to 200% above normal. Conversely, castration or antiandrogen administration to human males is not associated with a consistent decrease in aggression. Finally, changes in human aggression associated with neuropathology are not consistent with current knowledge of the neural basis of testosterone-dependent aggression. In contrast, human aggression does have a substantial number of features in common with defensive aggression seen in nonprimate mammals. It is present at all age levels, is displayed by both males and females, is directed at both males and females, and is not dependent on seasonal changes in hormone levels or experiential events such as sexual activity. As would be expected from current knowledge of the neural system controlling defensive aggression, aggression in humans increases with tumors in the medial hypothalamus and septal region, and with seizure activity in the amygdala. It decreases with lesions in the amygdala. The inference that human aggression has its roots in the defensive aggression of nonprimate mammals is in general agreement with evidence on the consistency of human aggressiveness over age, with similarities in male and female aggressiveness in laboratory studies, and with observations that some neurological disturbances contribute to criminal violence. This evidence suggests that human aggression has its biological roots in the defensive aggression of nonprimate mammals and not in hormone-dependent aggression based on testosterone.

Aggression↗
PubMed2002

Social and neural determinants of aggressive behavior: pharmacotherapeutic targets at serotonin, dopamine and gamma-aminobutyric acid systems.

BACKGROUND AND RATIONALE: Aggressive outbursts that result in harm and injury present a major problem for the public health and criminal justice systems, but there are no adequate treatment options. Obstacles at the level of social policy, institutional regulation, and scientific strategy in developing animal models continue to impede the development of specific anti-aggressive agents for emergency and long-term treatments. OBJECTIVE: To be more relevant to the clinical situation, preclinical aggression research has begun to focus on the neurobiological determinants of escalated aggressive behavior that exceeds species-typical patterns. It is the goal of this review to examine novel pharmacological and molecular tools that target the neural mechanisms for different kinds of aggressive behavior more selectively than previously possible and to outline potential pharmacotherapeutic options. RESULTS AND CONCLUSIONS: (1) The preclinical focus on the behavioral characteristics and determinants of intense aggression promises to be most relevant to the clinical distinction between the proposed impulsive-reactive-hostile-affective subtypes of human aggression and the controlled-proactive-instrumental-predatory subtypes of aggression. The neural circuits for many types of human and animal aggression critically involve serotonin, dopamine and gamma-aminobutyric acid (GABA) and specific receptor subtypes. (2) The dynamic changes in frontal cortical serotonin that are triggered by engaging in aggressive behavior imply that serotonergic drug effects are largely determined by the functional state of the receptors at the time of drug treatment. Of the numerous 5-HT receptors currently identified, the 5-HT(1B) receptors offer a promising target for reducing impulsive aggressive behavior, particularly if the action can be limited to sites in the central nervous system. (3) Aggressive confrontations are salient stressors, both for the aggressor as well as the victim of aggression, that are accompanied by activation of the mesocorticolimbic but not the striatal dopamine system. Dopaminergic manipulations, particularly targeting the D(2) receptor family, can influence aggressive behavior in animals and human patients, suggesting that mesocorticolimbic dopamine may have important enabling or permissive functions. (4) GABA is critical in the neurochemical control of aggressive behavior as evidenced by studies that directly modify GABAergic neurotransmission and neurochemical studies that correlate GABA measurements with aggressive behavioral responses in several animal species. The GABA(A) receptor complex is a mechanism through which certain benzodiazepines and alcohol enhance and inhibit aggressive behaviors. Social and pharmacological experiences decisively determine the effects of GABAergic positive modulators on aggression.

Adaptation, Psychological↗
PubMed2003

Interaction effects of corticosterone and experience on aggressive behavior in the green anole lizard.

Aggressive encounters are accompanied by a release of stress hormone, and this corticosterone (CORT) secretion could influence aggressive behavior in subsequent encounters. We investigated the modulating effects of CORT on aggressive behavior in the context of a 5-day social experience in male green anole lizards. In Experiment 1, we measured plasma CORT levels in animals that were exposed for different times to aggressive males. In Experiment 2, using metyrapone, a CORT synthesis blocker, we tested whether CORT secretion in response to the aggressive stimulus plays a role in experience-dependent facilitation of aggressive behavior. We hypothesized that aggressive encounters would increase plasma CORT levels, and that blocking CORT synthesis with metyrapone treatment during the aggressive encounter would cause an animal to become more aggressive. We also tested whether blocking CORT would interfere with the influence of 5-day social experience on animals' behavior in a subsequent aggressive encounter. Animals that were exposed to another male showed higher plasma CORT levels immediately after the 10 min encounter than animals exposed to the non-social video, and this high level was maintained through day 5. Within the aggressive video groups, in Experiment 2, there was a distinctly different pattern in displays depending on drug condition: vehicle-injected animals showed gradual increases followed by decreases in aggressive behavioral responses to the video as the five days proceeded (habituation), while animals injected with metyrapone started out with high aggressive behavior and did not decrease behavioral responses at later trials (no habituation). Finally, when tested with a novel conspecific on day 6, animals previously injected with metyrapone showed no higher aggression than did animals previously injected with vehicle and exposed to the aggressive video. These results suggest that blocking CORT synthesis during the exposure to the aggressive video induced animals to remain aggressive toward the repetitive stimulus without habituating, while not becoming more aggressive than controls toward a novel challenger.

Aggression↗
PubMed1997

Psychopharmacologic treatment of pathologic aggression.

Several drugs are apparently effective in treating pathologic anger and aggression. Because many of the studies on aggressive populations allowed the use of concomitant medications, it is unclear whether the efficacy of each drug in a particular population is dependent on the presence of other medications, such as antipsychotic agents. Finally, one needs to be circumspect in inferring efficacy of a particular drug in aggressive patients with neuropsychiatric conditions other than the ones in which some efficacy has been established. Lithium appears to be an effective treatment of aggression among nonepileptic prison inmates, mentally retarded and handicapped patients, and among conduct-disordered children with explosive behavior. Certainly, lithium would be the treatment of choice in bipolar patients with excessive irritability and anger outbursts, and it has been shown to be effective in this population. Anticonvulsant medications are the treatment of choice for patients with outbursts of rage and abnormal EEG findings. The efficacy of these drugs in patients without a seizure disorder, however, remains to be established, with the exception perhaps of valproate and carbamazepine. In fact, dyphenylhydantoin did not appear to be effective in treating aggressive behavior in children with temper tantrums and was found to be effective in only a prison population. There is some evidence for the efficacy of carbamazepine and valproate in treating pathologic aggression in patients with dementia, organic brain syndrome, psychosis, and personality disorders. As Yudofsky et al point out in their review of the literature, although traditional antipsychotic drugs have been used widely to treat aggression, there is little evidence for their effectiveness in treating aggression beyond their sedative effect in agitated patients or their antiaggressive effect among patients whose aggression is related to active psychosis. Antipsychotic agents appear to be effective in treating psychotic aggressive patients, conduct-disordered children, and mentally retarded patients, with only modest effects in the management of pathologic aggression in patients with dementia. Furthermore, at least in one study, these drugs were found to be associated with increased aggressiveness in mentally retarded subjects. On the other hand, atypical antipsychotic agents (i.e., clozapine, risperidone, and olanzapine) may be more effective than traditional antipsychotic drugs in aggressive and violent populations, as they have shown efficacy in patients with dementia, brain injury, mental retardation, and personality disorders. Similarly, benzodiazepines can reduce agitation and irritability in elderly and demented populations, but they also can induce behavioral disinhibition. Therefore, one should be careful in using this class of drugs in patients with pathologic aggression. Beta-blockers appear to be effective in many different neuropsychiatric conditions. These drugs seem effective in reducing violent and assaultive behavior in patients with dementia, brain injury, schizophrenia, mental retardation, and organic brain syndrome. As pointed out by Campbell et al in their review of the literature, however, systematic research is lacking, and little is known about the efficacy and safety of beta-blockers in children and adolescents with pathologic aggression. Although widely used in the management of pathologic aggression, the use of this class of drugs has been limited partially by marked hypotension and bradycardia, which are side effects common at the higher doses. The usefulness of the antihypertensive drug clonidine in the treatment of pathologic aggression has not been assessed adequately, and only marginal benefits were observed with this drug in irritable autistic and conduct disorder children. Psychostimulants seem to be effective in reducing aggressiveness in brain-injured patients as well as in violent adolescents with oppositional or conduct disorders, particu

Adrenergic beta-Antagonists↗
PubMed1996

A clinical approach to the pharmacotherapy of aggression in children and adolescents.

Overt aggression in its various forms is the most prevalent symptom presenting to pediatric mental health providers, regardless of setting. It is a behavior with a heterogeneous etiology and requires a comprehensive approach to evaluation and treatment. Evaluation of the aggressive child must assess medical, neurologic, psychiatric, psychosocial, familial, and/or educational contributions to behavioral dyscontrol. Multimodal treatment is generally required. At present, there is no single medication to recommend for the treatment of aggressive behavior. Multiple medications have clinically been used in a nonspecific fashion to target excessive childhood aggression. Although successful for some, this approach increases risk for ineffective interventions accompanied by side effects. Until a scientific understanding of the developmental neurobiology of aggression leads to more specific treatment, this review suggests the use of a diagnostic-based approach to the pharmacology of aggression (FIG. 1). Descriptive diagnostic techniques should be used to define the presence of any primary or comorbid psychiatric disorder that presents with aggression as an associated symptom. Treating aggression in the context of these psychiatric syndromes appears to be the most direct approach. Aggression occurring in the context of a medication-responsive psychiatric diagnosis appears most sensitive to pharmacologic intervention. Presently, evidence for efficacy is strongest for aggression in the context of ADHD, psychotic disorder, adolescent-onset bipolar disorder, and ictal aggression It remains less clear that medication can help aggression when it occurs independently of a pharmacologically treatable comorbid psychiatric disorder. Aggression may respond to a target symptom approach where discrete behavioral symptoms that contribute to aggression, such as irritability, explosiveness, fear, or impulsivity, may be modified by medication intervention (FIG. 1). When treatment is approached in this fashion, it is standard practice to use the least toxic and safest intervention first. Behavioral treatment based on contingency management principles could be initially recommended. Medication trials should first use medications that have demonstrated empiric efficacy in reducing aggression (TABLE 1) and that have a favorable safety profile. Neuroleptics to treat aggression in nonpsychotic psychiatrically referred youth should be kept to a minimum, secondary to their significant adverse risk profile. Alternative medications, such as selective serotonin reuptake-inhibiting antidepressants, buspirone, lithium, anticonvulsants, opiate blocking agents, propranolol, nadolol, and clonidine, deserve more clinical research in pediatric aggression. These medications may offer effective and less toxic alternatives in the pharmacologic treatment of inappropriate excessive childhood aggression.

Adolescent↗
PubMed2005

5-HT1A and 5-HT1B receptor agonists and aggression: a pharmacological challenge of the serotonin deficiency hypothesis.

More than any other brain neurotransmitter system, the indolamine serotonin (5-HT) has been linked to aggression in a wide and diverse range of species, including humans. The nature of this linkage, however, is not simple and it has proven difficult to unravel the precise role of this amine in the predisposition for and execution of aggressive behavior. The dogmatic view that 5-HT inhibits aggression has dominated both pharmacological research strategies to develop specific and effective novel drug treatments that reduce aggressive behavior and the pharmacological mechanistic interpretation of putative serenic drug effects. Our studies on brain serotonin and aggression in feral wild-type rats using the resident-intruder paradigm have challenged this so-called serotonin deficiency hypothesis of aggressive behavior. The well-known fact that certain 5-HT(1A/1B) receptor agonists potently and specifically reduce aggressive behavior without motor slowing and sedative effects is only consistent with this hypothesis under the assumption that the agonist mainly acts on the postsynaptic 5-HT(1A/1B) receptor sites. However, systemic injections of anti-aggressive doses of 5-HT(1A) and (1B) agonists robustly decrease brain 5-HT release due to their inhibitory actions at somatodendritic and terminal autoreceptors, respectively. The availability of the novel benzodioxopiperazine compound S-15535, which acts in vivo as a preferential agonist of the somatodendritic 5-HT(1A) auto-receptor and as an antagonist (weak partial agonist) at postsynaptic 5-HT(1A) receptors, allows for a pharmacological analysis of the exact site of action of this anti-aggressive effect. It was found that, similar to other prototypical full and partial 5-HT(1A) and/or 5-HT(1B) receptor agonists like repinotan, 8-OHDPAT, ipsapirone, buspirone, alnespirone, eltoprazine, CGS-12066B and CP-93129, also S-15535 very effectively reduced offensive aggressive behavior. Unlike the other ligands, however, a remarkable degree of behavioral specificity was observed after treatment with S-15535, in that the anti-aggressive effects were not accompanied by inhibiting (like other 5-HT(1A) receptor agonist with moderate to high efficacy at postsynaptic 5-HT(1A) receptors) or enhancing (like agonists with activity at 5-HT(1B) receptors and alnespirone) non-aggressive motor behaviors (e.g., social exploration, ambulation, rearing, and grooming) beyond the range of undrugged animals with corresponding levels of aggression. The involvement of 5-HT(1A) and/or 5-HT(1B) receptors in the anti-aggressive actions of these drugs was convincingly confirmed by showing that the selective 5-HT(1A) receptor antagonist WAY-100635 and/or the 5-HT(1B) receptor antagonist GR-127935, while inactive when given alone, effectively attenuated/prevented these actions. Furthermore, combined administration of S-15535 with either alnespirone or CGS-42066B elicited a clear additive effect, indicated by a left-ward shift in their dose-effect curves, providing further support for presynaptic sites of action (i.e., inhibitory somatodendritic 5-HT(1A) and terminal 5-HT(1B) autoreceptors). These findings strongly suggest that the specific anti-aggressive effects of 5-HT(1A) and 5-HT(1B) receptor agonists are predominantly based on reduction rather than enhancement of 5-HT neurotransmission during the combative social interaction. Apparently, normal display of offensive aggressive behavior is positively related to brief spikes in serotonergic activity, whereas an inverse relationship probably exists between tonic 5-HT activity and abnormal forms of aggression only.

Aggression↗
PubMed2003

Problems in the study of rodent aggression.

Laboratory research has produced detailed descriptions of aggression and defense patterns in the rat, mouse, and hamster, showing strong similarities, but also some differences, across these species. Research on target sites for attack, in conjunction with analyses of the situational antecedents of attack behaviors and of responsivity of these to conditions that elicit fear, has also provided a strong basis for analysis of offensive and defensive aggression strategies and for identification of combinations of these modalities such as may occur in maternal aggression. These patterns have been empirically differentiated from phenomena such as play fighting or predation and compared for laboratory rodents and their wild ancestors. An array of tasks, suitable for use with pharmacological and experimental manipulations, is available for analysis of both aggression and defense. These developments should produce a firm basis for research using animal models to analyze a broad array of aggression-related phenomena, including systematic approaches to understanding the normal antecedents and consequences of each of several differentiable types of aggressive behavior. Despite this strong empirical and analytic background, laboratory animal aggression research has been in a period of decline, spanning several decades, relative to comparable research focusing on areas such as sexual behavior or stress. Problems that may have contributed to the relative neglect of aggression research include confusion about the interpretation of different tasks for eliciting aggression; difficulties and labor intensiveness of observational measures needed for an adequate differentiation of offensive and defensive behaviors; analytic difficulties stemming from the sensitivity of offensive aggression to the inhibitory effects of fear or defensiveness; lack of a clear relationship between categories of aggressive behavior as defined in animal studies and those used in human aggression research; and the social and political difficulties undermining support for research on a topic that, when applied to humans, provides a stigmatizing label. While all of these provide some rationale for eschewing aggression research, aggression remains a serious social, economic, health, and political problem. The neglect of research in this area contributes to an ongoing failure to understand the degree of similarity across mammalian species in the antecedents, neural systems, behavioral expression, and outcomes of aggression. This failure, in turn, hinders analyses of normal and abnormal forms of aggression and of the appropriate roles of the former in society, reducing the possibility of sensitive and effective approaches to control inappropriate human aggressive behaviors.

Aggression↗
PubMed2003

Aggression on a psychiatric acute ward: a three-year prospective study.

The objectives of this 3-yr. prospective study of aggression on a Norwegian psychiatric acute ward serving a population of 170,000 were to monitor the rate and characteristics of aggressive behaviour, to identify possible interactional and situational precipitants to aggression, and to explore possible differences between aggressive and nonaggressive patients in terms of diagnosis, sex, age, numbers of admissions, admission type, and length of stay. Aggressive incidents were recorded on the Report Form for Aggressive Episodes (REFA). Severity of injuries was scored according to Fottrell's severity scale. Of the total 934 patients admitted, 98 (10.5%) accounted for a total of 981 aggressive episodes. About 55% of the aggressive incidents were assaults that resulted in 85 minor and 21 severe physical injuries. There was no evidence that diagnosis might be used to predict aggression in the clinical setting. Mean rate of admission per patient and length of stay was significantly higher in the aggressive group than in the nonaggressive group. However, several patients in the aggressive group also had admissions without being aggressive. About 13% of the aggressive patients accounted for nearly 50% of the aggressive incidents. There was no significant sex difference by total rate of aggression, but female patients tended to have higher rates of assaults and contributed to significantly more injuries than male patients. Nearly 20% of the aggressive episodes occurred during the first 24 hours of a stay and 54% during the first week. Limit setting, problems in communication, and physical contact, separately or in combinations, preceded nearly 90% of the aggressive episodes.

Acute Disease↗
PubMed1999

Female territorial aggression and steroid hormones in mountain spiny lizards.

In certain species, females are highly aggressive. For example, female mountain spiny lizards, Sceloporus jarrovi, express aggressive behaviours when defending their territories. Despite the occurrence of female aggression, relatively little is known about its underlying hormonal mediation. As a first step in understanding neuroendocrine mechanisms of female aggression, this study documented seasonal changes in territorial aggression, plasma steroid hormone levels, and reproductive condition in free-living female mountain spiny lizards. We determined how seasonal patterns of testosterone (T), oestradiol (E), dihydrotestosterone (DHT) and corticosterone (B) corresponded to seasonal patterns of aggression. At times of the year when females were most aggressive, plasma levels of T and E were elevated. At times of the year when females were least aggressive, plasma B was elevated. Furthermore, when levels of T were elevated, females were more aggressive, and when levels of B were elevated, females were less aggressive. Plasma levels of DHT were not associated with aggression. These seasonal patterns are consistent with the hypotheses that T, and perhaps E, promote female aggression, while B suppresses female aggression. Despite these associations of hormones and aggression, no hormone was associated with aggression in a one-to-one fashion. This suggests that if steroid hormones contribute to the expression of female aggression, they must interact with each other or with other factors (for example, other hormones, receptor levels, environmental factors) to mediate fully the expression of aggression. Copyright 1999 The Association for the Study of Animal Behaviour.

Journal Article↗
PubMed1994

The relationship between aggressive behavior and puberty in normal adolescents: a longitudinal study.

PURPOSE: To assess changes in aggressive behaviors as related to progression from early to late puberty in normal adolescents. METHODS: Subjects were normal English schoolchildren. An observational cohort design was employed. Pubertal status was measured by Tanner staging. Self-reports of verbal aggression against adults, physical aggression against peers, aggressive impulses and aggressive inhibitory responses, were collected at three points in time. Analyses were performed for the entire group of 106 subjects in 1983, 77 subjects in 1985 and 70 subjects in 1987. Statistical methods included analysis of variance, regression and correlation and cluster formation. RESULTS: There were decreases in all aggression variables except in aggressive impulses over this time period. When analyzed by gender, boys were initially more aggressive than girls, but by late puberty all gender differences in self-reported aggressive behaviors had disappeared. When only those subjects who were evaluated at all three data collection times were grouped by similar responses on both aggression and physical variables, three clusters of boys and girls were identified. Clusters contained varying proportions of boys and girls. Cluster one (48.5% of the entire sample) was a low aggression group. Cluster two (30.3%) was a high aggression group, and cluster three (21.2%) was an intermediate aggression group. These clusters seemed to have relatively stable aggression characteristics over time. CONCLUSIONS: These data suggest that groups of boys and girls who report similar aggression characteristics and have similar growth and pubertal characteristics can be identified. Neither gender alone, nor pubertal status alone, nor by inference, hormones alone is sufficient to explain the complex set of behaviors which are involved in aggression.

Adolescent↗
PubMed2005

Escalated aggressive behavior: dopamine, serotonin and GABA.

The ethical dilemma in aggression research is how to reconcile two divergent objectives, namely to avoid harm and injury as much as possible and, at the same time, how to study behavioral phenomena that validly represent the essence of the neurobiology of aggression. Clinical and preclinical aggression research focuses on different types of aggression. Preclinical studies are usually stimulated by an ethological approach and focus on the phylogeny, ontogeny, survival value and neural mechanisms of ritualized displays and signals. On the other hand, clinical studies focus on violent individuals and pathologically excessive forms of aggressive behavior. This review emphasizes research on escalated forms of aggression in animals and humans and their pharmacotherapy. The current experimental models to generate escalated levels of aggressive behavior in laboratory rely on social instigation, frustrative non-reward and alcohol drinking. These types of aggression are modulated by canonical neurotransmitters like dopamine, serotonin (5-HT) and GABA. It continues to be a main goal of much neurobiological research to find potential targets of pharmacological agents that interact with dopaminergic, GABAergic and serotonergic systems and have high efficacy and selectivity to reduce excessive levels of aggressive and violent behaviors without side-effects. While the mesocorticolimbic dopamine system is implicated in the initiation, execution, termination and consequences of aggressive behavior, drugs with a high affinity for dopamine D2 receptors lack specificity for reducing aggressive behavior. Current investigations point to 5-HT(1B) receptor subtypes as particularly relevant. First, they are differentially expressed in aggression-prone individuals relative to those who are not excessively aggressive. Second, these and also other 5-HT receptor subtypes emerge to be significant targets for anti-aggressive interventions. Positive modulators of GABA(A) receptors with specific subunit configuration may be relevant for heightening aggression, and these sites may be targets for intervention. A prerequisite for rational pharmacotherapies will be adequate characterization of serotonergic and GABAergic receptor regulation in individuals exhibiting escalated aggression.

Aggression↗
PubMed2003

Effects of diazepam and flumazenil on food competition behavior in high- and low-aggression pigeons.

The food competition interaction test performed with food-restricted pigeons with previously consolidated dominance is a useful tool for the study of offensive and defensive social aggression. In the present study, we examined the effect of GABA-A-benzodiazepine (BZD) receptor manipulation on aggression, emotion, feeder control, and eating behavior in high- and low-aggression female pigeons maintained at 80% of their normal weight and exposed to food competition interactions. The pigeons were divided into pairs by previously ranked high-aggression females (total time spent in aggression over 60 s/5 min; n=6 pairs) and low-aggression females (time spent in aggression less than 10 s/5 min; n=6 pairs). In Experiment 1, a pigeon in each pair of high- and low-aggression subjects were treated daily with an oral dose of diazepam (DZP, 0.6 mg/kg/0.3 ml) for 8 days. The other animal received the vehicle. On Day 8, food competition trials (10 min) were performed 30 min after treatments. In Experiment 2, pigeons were injected subcutaneously with flumazenil (FZL, 0.1 mg/kg/1 ml) or saline and exposed to a food competition trial 30 min after injections. In Experiment 3, one animal in each pair received DZP for 8 days. The other animal received the vehicle. On Day 8, the DZP-treated subjects were injected subcutaneously with FZL (0.1 mg/ kg/1 ml) 30 min before the oral dose of DZP. Trials were performed 30 min after DZP or vehicle administration. In Experiment 1, it was found that the DZP group of high-aggression pigeons showed lower scores of aggression (P<.05) and emotional responses (P<.05) than controls. The other group-scored behaviors were not affected. The DZP low-aggressions, however, showed scores of aggression eightfold higher than their controls (P<.05) but the other scored behaviors were not changed. In Experiment 2, FZL injection did not induce intrinsic effects on aggression either in the high- or in the low-aggression group. Experiment 3 showed that the emotional and aggressive responses to DZP were neutralized by FZL. This shows that GABA-A-BZD receptor mechanisms are implicated in the DZP responses in high- and low-aggression pigeons.

Aggression↗
PubMed1997

The neurobiology of impulsive aggression.

As noted previously, it is likely that the tendency to lash out verbally or physically at others is influenced by an interaction among multiple complex biologic factors. We need to investigate how these systems interact with each other to develop a more thorough understanding of the brain's influence over aggressive behavior. We are at a very early stage in our understanding of the neurobiology of aggression. There are no simple tools for studying the complex neurophysiology of the human brain. The studies cited in this article include techniques limited in their utility. As our technologies improve, discovering a more thorough picture of the brain's influence over aggressive behavior may be possible. For example, functional neuroimaging may help to localize abnormal neurotransmitter functioning in the brains of individuals with impulsive aggressive behavior. Our technologies are beginning to reveal the differential effects of subsystems of neurotransmitter regulation. Subtypes of serotonin receptors may differentially mediate impulsive aggressive behaviors. Animal studies suggest that 5-HT 1A receptor stimulation results in a decrease in aggressive behavior. As noted previously, aggressive personality-disordered patients show a blunted prolactin response to the 5-HT1A agonist buspirone. Antagonism of 5-HT 2 receptors appears to decrease aggression, and this effect may explain the ability of newer antipsychotic agents (which, unlike older antipsychotic medications, block 5-HT 2 receptors) to produce a dramatic reduction in aggression and agitation independent of effects on psychotic symptoms. Neglecting psychosocial factors in the causes of aggressive behavior would also be naive. Although environmental factors account for much of the predisposition to aggression, there have been few systematic studies to explore the relationship between life experiences and aggression. In addition, there have been no well-designed studies of the interaction between biology and an individual's environment in the genesis of aggressive behavior. There is some evidence of an association between childhood abuse and neglect and adult antisocial personality disorder, but this relationship might be merely an artifact of the genetic relationship between parental and offspring antisocial personality disorder. As we discussed in the introduction, one of the biggest hurdles in the study of the neurobiology of aggression is the lack of a consensus on definitions. "Intermittent Explosive Disorder" is the only category in DSM-IV that directly addresses individuals with problems with aggression, but the criteria are vague and only focus on a handful of the many patients who exhibit problems with aggressive behavior. It is our hope that investigators in this field can work together toward developing more precise and encompassing diagnostic criteria to study effectively both the neurobiology and treatment of these disorders.

Aggression↗
PubMed1999

Developmental exposure to vasopressin increases aggression in adult prairie voles.

Although the biological roots of aggression have been the source of intense debate, the precise physiological mechanisms responsible for aggression remain poorly understood. In most species, aggression is more common in males than females; thus, gonadal hormones have been a focal point for research in this field. Although gonadal hormones have been shown to influence the expression of aggression, in many cases aggression can continue after castration, indicating that testicular steroids are not completely essential for the expression of aggression. Recently, the mammalian neuropeptide arginine vasopressin (AVP) has been implicated in aggression. AVP plays a particularly important role in social behavior in monogamous mammals, such as prairie voles (Microtus ochrogaster). In turn, the effects of social experiences may be mediated by neuropeptides, including AVP. For example, sexually naïve prairie voles are rarely aggressive. However, 24 h after the onset of mating, males of this species become significantly aggressive toward strangers. Likewise, in adult male prairie voles, central (intracerebroventricular) injections of AVP can significantly increase intermale aggression, suggesting a role for AVP in the expression of postcopulatory aggression in adult male prairie voles. In this paper, we demonstrate that early postnatal exposure to AVP can have long-lasting effects on the tendency to show aggression, producing levels of aggression in sexually naïve, adult male prairie voles that are comparable to those levels observed after mating. Females showed less aggression and were less responsive to exogenous AVP, but the capacity of an AVP V(1a) receptor antagonist to block female aggression also implicates AVP in the development of female aggression.

Aggression↗
PubMed2004

Which types of aggressive behaviour are associated with suicidal and self-injurious behaviour at the time of admission?

BACKGROUND: In psychiatry and psychotherapy, dealing with aggressiveness and autoaggressiveness is of great importance. Our aim was to find a link between overt aggressive and autoaggressive behaviour, which could be readily observed. SAMPLING AND METHODS: We investigated the frequency, type and intensity of aggressive, suicidal and self-injurious behaviour exhibited by 521 successively admitted psychiatric patients at the time of admission with the help of a standardised instrument (Social Dysfunction and Aggression Scale). The Social Dysfunction and Aggression Scale enables the investigation of 9 different types of overt aggressive behaviour and 2 different types of autoaggressive behaviour (suicidal vs. self-injurious behaviour). After calculating correlations between single variables, we attempted to estimate the predictive value of the different types of aggressive behaviour for suicidal and self-injurious behaviour by using ordinal regression models. In addition, the categorical information of our data was evaluated by loglinear analyses. RESULTS: Our study showed that all degrees of aggressiveness (low, moderate, high), which are exhibited in different types of aggressive behaviour, were linked to an increased risk of self-injurious behaviour. No correlation was found, however, between overt aggressive behaviour and suicidal behaviour. Only in the subgroup of depressive disorders did we establish that the risk of aggressive behaviour was decreased and the risk of suicidal behaviour was increased at the time of admission. CONCLUSIONS: The strong relationship between aggressive behaviour and self-injurious behaviour has previously been described in specific diagnostic subgroups, but not yet in a heterogeneous population of psychiatric in-patients from a defined catchment area. We, therefore, conclude that the link between aggressive and self-injurious behaviour could be a general one. Exhibiting aggressive behaviour and self-injurious behaviour within a short time span may be the result of an increased or disinhibited aggressive potential, which is independent of a specific diagnosis. As such, it possibly represents the general consequence of a highly altered state of mind and does not seem to be linked to a specific diagnostic subgroup. In psychiatric emergency situations, the previously described close relationship between aggressive and self-injurious behaviour should be taken into account.

Adolescent↗
PubMed1987

[Motives and interpersonal functions of aggression].

In this review, the author theoretically and empirically examined motives and interpersonal functions of aggression. A factor-analysis of Averill's questionnaire items on anger revealed that motives involved in aggressive responses were clustered into two groups: the hostile and the instrumental. It was also clarified that an individual is likely to engage in aggression particularly when some hostile motives are evoked. Concerning the interpersonal functions, the author proposed that aggression might serve four principal goals. (1) Aggression can be generated as an avoidance response to an aversive stimulus, such as frustration, annoyance, or pain, and so on. It depends on the severity of the stimulus. It was however emphasized that aggression is also mediated by social cognition, such as an attribution of intent to a harm-doer. (2) Aggression can be used as a means of coercing the other person into doing something. An individual is likely to use such a power strategy if he/she is lacking in self-confidence or a perspective for influencing the target person by more peaceful strategies. (3) Aggression can be interpreted as a punishment when it is directed toward a transgressor. In this case, aggression is motivated by restoration of a social justice, and thus its intensity is determined by the perceived moral responsibility of the transgressor. Further, it was indicated that aggression is intensified if it is justified as a sanctional conduct against the immoral. (4) Aggression can be also evoked when an individual's social identity is threatened. It was suggested that impression management motives are involved in aggression by an unexpected finding that the presence of audience or the identifiability rather facilitated retaliative aggression. The aggression-inhibition effect of apology was also explained in terms of impression management. In conclusion, it was presented that aggression is a behavioral strategy as an attempt to resolve interpersonal conflicts including physical or psychological annoyance, the other person's disobedience, perceived injustice, and a threat to one's social identity. Whether one's aggression is performed or not depends on a number of intra- and inter-personal determinants, particularly on social cognitive processes such as attribution, inference, prediction and other judgements.

Aggression↗
PubMed1985

Maternal aggression in rats: effects of chlordiazepoxide and fluprazine.

Although maternal aggression in rats is confined to a restricted post-partum period, the high and stable aggression level and the constancy of its behavioural structure make it an attractive experimental procedure for studying the behavioural effects of psychotropic drugs. Female rats were tested against naive male intruder rats for 5 or 10 min on post-partum days 3-9, during which aggression is stable. Chlordiazepoxide (CDP; 5, 10 and 20 mg/kg, orally) had a biphasic effect on aggression; it increased aggression considerably at 5 and (to a lesser extent) at 10 mg/kg. At 20 mg/kg aggression returned to control level. CDP shortened the latency to the first attack at 5 mg/kg, but not at higher dosages. CDP enhanced aggression, particularly in the first 2 min of an encounter. It did not change the structure of the aggressive behaviour, but did induce a dose-dependent increase in feeding. Fluprazine (Flu; 5, 10 and 20 mg/kg IP), a specific antiaggressive (serenic) drug, induced a dose-dependent decrease in aggression and exerted its largest effect in the first 2 min of an encounter. In accordance with the reduced aggression, latencies to the first attack increased. Maternal aggression in rats represents an extension to other (male) aggression paradigms in psychopharmacology. First, it has no male counterpart. Secondly, the hormonal mechanisms underlying this behaviour differ from those of male aggression. Thirdly, the morphology of maternal aggression is different from that shown in male models of agonistic behaviour (e.g. resident-intruder). These features make maternal aggression an attractive paradigm for pharmacological studies of female behaviour.

Aggression↗
PubMed1993

Instrumental and hostile aggression in childhood disruptive behavior disorders.

An analogue task of instrumental and hostile aggression during a competitive game was evaluated in a sample of clinically-referred 8- to 12-year-old aggressive boys. Similar to a prior task in a normative sample (Hoving, Wallace, & La Forme, 1979), both types of aggression increased during provocation as compared to baseline, indicating the success of the provocation manipulation, with moderate correlations between the two aggressive responses. The aggressive group with attention-deficit hyperactivity disorder (ADHD) and the aggressive group without ADHD each had higher rates of instrumental aggression than controls. Only the aggressive/ADHD group had higher rates of hostile aggression than controls. Parent Child Behavior Checklist ratings indicated a modest but significant unique relationship between instrumental aggression and delinquency. The high rate of both types of aggression in the aggressive/ADHD group suggests that comorbid ADHD and aggression may result in qualitative differences in aggressive behavior. The high rate of hostile aggression in the aggressive-ADHD group supports theoretical assumptions regarding the relationship of hostile aggression to poor impulse control.

Aggression↗