Individual Differences In Aggressive Behavior Research Articles

Structural covariance of amygdala subregions is associated with trait aggression and endogenous testosterone in healthy individuals

Many studies point toward volume reductions in the amygdala as a potential neurostructural marker for trait aggression. However, most of these findings stem from clinical samples, rendering unclear whether the findings generalize to non-clinical populations. Furthermore, the notion of neural networks suggests that interregional correlations in gray matter volume (i.e., structural covariance) can explain individual differences in aggressive behavior beyond local univariate associations. Here, we tested whether structural covariance between amygdala subregions and the rest of the brain is associated with self-reported aggression in a large sample of healthy young students (n = 263; 49% women). Salivary testosterone concentrations were measured for a subset of n = 40 male and n = 36 female subjects, allowing us to investigate the influence of endogenous testosterone on structural covariance. Aggressive individuals showed enhanced covariance between left superficial amygdala (SFA) and left dorsal anterior insula (dAI), but lower covariance between right laterobasal amygdala (LBA) and right dorsolateral prefrontal cortex (dlPFC). These structural patterns overlap with functional networks involved in the genesis and regulation of aggressive behavior, respectively. With increasing endogenous testosterone, we observed stronger structural covariance between right centromedial amygdala (CMA) and right medial prefrontal cortex in men and between left CMA and bilateral orbitofrontal cortex in women. These results speak for structural covariance of amygdala subregions as a robust correlate of trait aggression in healthy individuals. Moreover, regions that showed structural covariance with the amygdala modulated by either testosterone or aggression did not overlap, suggesting a complex role of testosterone in human social behavior beyond facilitating aggressiveness.

Polygenic risk for aggressive behavior from late childhood through early adulthood.

Twin studies suggest a substantial role for genes in explaining individual differences in aggressive behavior across development. It is unclear, however, how directly measured genetic risk is associated with aggressive behavior at different moments across adolescence and how genes might distinguish developmental trajectories of aggressive behavior. Here, a polygenic risk score derived from the EAGLE-Consortium genome-wide association study of aggressive behavior in children was tested as predictor of latent growth classes derived from those measures in an adolescent population (n = 2229, of which n = 1246 with genetic information) and a high-risk sample (n = 543, of which n = 335 with genetic information). In the population sample, the polygenic risk score explained variation in parent-reported aggressive behavior at all ages and distinguished between stable low aggressive behavior and moderate and high-decreasing trajectories based on parent-report. In contrast, the polygenic risk score was not associated with self- and teacher-reported aggressive behavior, and no associations were found in the high-risk sample. This pattern of results suggests that methodological choices made in genome-wide association studies impact the predictive strength of polygenic risk scores, not just with respect to power but likely also in terms of generalizability and specificity.

A genome-wide approach to children's aggressive behavior: The EAGLE consortium.

Individual differences in aggressive behavior emerge in early childhood and predict persisting behavioral problems and disorders. Studies of antisocial and severe aggression in adulthood indicate substantial underlying biology. However, little attention has been given to genome-wide approaches of aggressive behavior in children. We analyzed data from nine population-based studies and assessed aggressive behavior using well-validated parent-reported questionnaires. This is the largest sample exploring children's aggressive behavior to date (N = 18,988), with measures in two developmental stages (N = 15,668 early childhood and N = 16,311 middle childhood/early adolescence). First, we estimated the additive genetic variance of children's aggressive behavior based on genome-wide SNP information, using genome-wide complex trait analysis (GCTA). Second, genetic associations within each study were assessed using a quasi-Poisson regression approach, capturing the highly right-skewed distribution of aggressive behavior. Third, we performed meta-analyses of genome-wide associations for both the total age-mixed sample and the two developmental stages. Finally, we performed a gene-based test using the summary statistics of the total sample. GCTA quantified variance tagged by common SNPs (10-54%). The meta-analysis of the total sample identified one region in chromosome 2 (2p12) at near genome-wide significance (top SNP rs11126630, P = 5.30 × 10(-8) ). The separate meta-analyses of the two developmental stages revealed suggestive evidence of association at the same locus. The gene-based analysis indicated association of variation within AVPR1A with aggressive behavior. We conclude that common variants at 2p12 show suggestive evidence for association with childhood aggression. Replication of these initial findings is needed, and further studies should clarify its biological meaning. © 2015 Wiley Periodicals, Inc.

Genetic variations in the serotoninergic system and environmental factors contribute to aggressive behavior in Chinese adolescents

Aggressive behavior is a major public health problem worldwide and has been associated with many gene variants, especially those related to the serotonin (5-hydroxytryptamine, 5-HT) system, and environmental factors. However, the overall contribution of serotonin-related genes to aggressive behavior is not well understood. With a sample of 478 healthy Chinese volunteers, this study investigated the relation between aggressive behavior and genetic variations of the serotoninergic system (as characterized by 129 representative polymorphisms) interacting with environmental factors (parental warmth and acceptance; stressful life events). We adopted a system-level approach to identify SNPs and environmental factors associated with aggressive behavior, and estimated their overall contribution to aggressive behavior using multiple regression, which was then verified by permutation analysis. We identified 12 SNPs that made statistically significant contributions to aggressive behavior. Next, main effects, interactions among these SNPs, and interactions between these SNPs and environmental factors were assessed using multiple regression. The final model accounted for approximately 19% of the variance for aggressive behavior. Permutation analysis confirmed that the probability of obtaining these findings by chance was low (p=0.045, permuted for 1000 times). These results showed that genetic variations in the serotoninergic system, combined with environmental risk factors, made a moderate contribution to individual differences in aggressive behavior among a healthy population sample.

Developmental constraints on behavioural flexibility

We suggest that variation in mammalian behavioural flexibility not accounted for by current socioecological models may be explained in part by developmental constraints. From our own work, we provide examples of constraints affecting variation in behavioural flexibility, not only among individuals, but also among species and higher taxonomic units. We first implicate organizational maternal effects of androgens in shaping individual differences in aggressive behaviour emitted by female spotted hyaenas throughout the lifespan. We then compare carnivores and primates with respect to their locomotor and craniofacial adaptations. We inquire whether antagonistic selection pressures on the skull might impose differential functional constraints on evolvability of skulls and brains in these two orders, thus ultimately affecting behavioural flexibility in each group. We suggest that, even when carnivores and primates would theoretically benefit from the same adaptations with respect to behavioural flexibility, carnivores may nevertheless exhibit less behavioural flexibility than primates because of constraints imposed by past adaptations in the morphology of the limbs and skull. Phylogenetic analysis consistent with this idea suggests greater evolutionary lability in relative brain size within families of primates than carnivores. Thus, consideration of developmental constraints may help elucidate variation in mammalian behavioural flexibility.

A Potential Role for a Genetic Variation of AKAP5 in Human Aggression and Anger Control

The A-kinase-anchoring protein 5 (AKAP5), a post-synaptic multi-adaptor molecule that binds G-protein-coupled receptors and intracellular signaling molecules has been implicated in emotional processing in rodents, but its role in human emotion and behavior is up to now still not quite clear. Here, we report an association of individual differences in aggressive behavior and anger expression with a functional genetic polymorphism (Pro100Leu) in the human AKAP5 gene. Among a cohort of 527 young, healthy individuals, carriers of the less common Leu allele (15.6% allele frequency) scored significantly lower in the physical aggression domain of the Buss and Perry Aggression Questionnaire and higher in the anger control dimension of the state-trait anger expression inventory. In a functional magnetic resonance imaging experiment we could further demonstrate that AKAP5 Pro100Leu modulates the interaction of negative emotional processing and executive functions. In order to investigate implicit processes of anger control, we used the well-known flanker task to evoke processes of action monitoring and error processing and added task-irrelevant neutral or angry faces in the background of the flanker stimuli. In line with our predictions, Leu carriers showed increased activation of the anterior cingulate cortex (ACC) during emotional interference, which in turn predicted shorter reaction times and might be related to stronger control of emotional interference. Conversely, Pro homozygotes exhibited increased orbitofrontal cortex (OFC) activation during emotional interference, with no behavioral advantage. Immunohistochemistry revealed AKAP5 expression in post mortem human ACC and OFC. Our results suggest that AKAP5 Pro100Leu contributes to individual differences in human aggression and anger control. Further research is warranted to explore the detailed role of AKAP5 and its gene product in human emotion processing.

Androgen levels and anger and impulsivity measures as predictors of physical, verbal and indirect aggression in boys and girls

Previous studies indicate that androgen levels and certain psychological characteristics such as anger and impulsivity are related to the development and maintenance of aggression. Further studies are required to analyze the potential predictor role of the interaction of said factors on aggressive behavior. 90 nine-year-old children (44 boys and 46 girls) were assessed in relation to their levels of physical, verbal and indirect aggression, using a peer-rating technique. Testosterone and androstenedione levels were analyzed using an enzymoimmunoassay technique in saliva samples. Anger (state and trait) and anger control were measured using the STAXI-NA, and impulsivity was measured through the MFF-20. A General Linear Model revealed that sex was the best predictor for aggression measures, with boys scoring higher than girls in physical, verbal and indirect aggression; after sex, testosterone was found to be the best predictor (in a positive sense) of all three types of aggressive behavior studied. In addition to observing a main effect of androstenedione on physical and verbal aggression, a 'state anger*androstenedione' interaction was found to predict these types of aggression, with androstenedione acting as a moderator (inhibitor) of the effects of anger on these behaviors; also, a 'state anger*testosterone' interaction was found to predict verbal aggression. The results support the idea that, after sex, androgens constitute a biological marker to be taken into consideration in relation to individual differences in aggressive behavior. It is possible that at the age of 9, testosterone tends to increase aggression, while androstenedione tends to moderate (inhibit) the effects of anger on aggression.

INNOVATIVE BUT INSUFFICIENT? A RESPONSE TO GRAHAM'S COMMENTARY ON ‘ALCOHOL, SUPPRESSED ANGER AND VIOLENCE’

We wish to thank Kate Graham for her comments [1] on our paper [2] and to respond to the issues that she raised. To recapitulate, by applying the first-difference (FD) method we submitted the alcohol–violence association to a more stringent test for causality than those used in previous survey research. Thus, using two-wave panel data from a general population study of young people, we estimated how changes in the frequency of violence correlated with changes in drinking. Further, we examined whether this correlation was contingent upon suppressed anger. The results indicated that alcohol may indeed be related causally to violence, but that the effect of drinking was confined to individuals who tend to withhold their angry feelings. Graham describes our study as innovative, but she also questions our statistical approach as well as our conclusion regarding the moderating role of suppressed anger. The major advantage of the FD-method is that it eliminates the effects of time-invariant confounders, but as Graham rightly points out, this method also has some important limitations. However, most of these limitations work in the direction of increasing the risk of type 2 error (rejecting a true hypothesis), which must be weighed against the reduced risk of type 1 error (not rejecting a false hypothesis). In his instructive methodology book, Firebaugh [3] notes that the first-difference method is conspicuously under-utilized in social science and pleads for a wider use of it. In response to some more technical queries, we wish to clarify that the log-transformation of our measures on alcohol use and violent behaviour was performed to linearize the associations between the two. There are certainly other transformations that could do this job, but logging has the advantage that it yields a highly intelligible effect measure (elasticity). Further, with regard to the items used to assess suppressed anger, Graham asks why we used factor scores rather than a sum score. Our answer is simple: factor scores are advantageous because each item contributes to the scale in proportion to its relation to the underlying dimension. Moreover, the fine-grained scale of the factor scores made it possible to divide our sample into three equal-sized groups, whereas the coarse summed scale yielded groups that differed substantially in numbers. It may also be noted that we used a sum score in the first version of our paper, yielding an identical pattern of findings to that observed when factor scores were applied instead. Graham also asks why Pearson's r was used to estimate cross-sectional correlations while the associations between the change scores were reported as elasticities. However, we did in fact also report cross-sectional elasticities (in addition to the Pearson's r), noting that these were twice the size of the elasticities based on change scores. According to Graham, the suppressed anger explanation that we propose may not apply to alcohol-related violence among young people. Referring to qualitative studies of bar-room aggression, she suggests that violent behaviour in relation to drinking may occur because it is considered normative among young males—not because withheld feelings of anger are more likely to be behaviourally expressed under the influence of alcohol. Indeed, for some subgroups of young males, this may well be the case. However, our study was based on a general population sample and we did not focus specifically on male-to-male aggression in the context of on-premise drinking. Moreover, only a tiny fraction of all drinking events (including those of young males) involves violence, and we examined whether alcohol in combination with the disposition to suppress anger could account for individual differences in aggressive behaviour. For both males and females, our hypothesis of a moderating role of this anger dimension was supported. Graham also suggests that the above-mentioned effect of suppressed anger may be due to other dimensions of anger or to an angry disposition more generally. However, we focused specifically upon suppressed anger because it was the theoretically more interesting one (e.g. fitting well into the disinhibition perspective), and allowed ourselves to do so because our analyses indicated that it was empirically distinctive from other indicators of anger. We still agree with Graham that a more convincing strategy would be to conduct comparable analyses for both suppressed and expressed anger. However, we do not agree that our findings are inconsistent with experimental research showing no moderating role of suppressed anger on the link between alcohol consumption and anger expression. Thus, the one and only study that Graham refers to in this context [4] used facial expression of anger as outcome measure, implying that its scope differed from that of our study. None.

Aggression, Digit Ratio and Variation in Androgen Receptor and Monoamine Oxidase A Genes in Men

Variation in prenatal exposure to androgens is thought to be responsible for some of the individual differences in aggressive behavior among adults. A putative indicator of prenatal testosterone exposure, 2D:4D (the index to ring finger length) ratios have shown a weak correlation with aggression. Variation in sensitivity of the androgen receptor, resulting from polymorphism in the AR gene, is also thought to influence the relative expression of sexually dimorphic traits within each sex, including aggressive behavior and 2D:4D. Here we examine variation in aggression, 2D:4D, and polymorphism in the AR and MAO-A genes in a sample of 188 men. We find no evidence of AR gene influence on right hand 2D:4D, and a weak trend towards more feminine-typical left hand 2D:4D in men with more sensitive androgen receptors. Men with more sensitive androgen receptors tended to score lower on many of the subscales of the Aggression Questionnaire and Indirect Aggression Questionnaire. We found no influence of MAO-A allele on either digit ratio or aggressive behavior. We conclude that more masculine-typical 2D:4D does not reflect greater sensitivity to testosterone through variation in this locus on the AR gene, and that AR alleles conferring greater sensitivity to testosterone are associated with lower, not higher propensity to aggression.

Motivational and situational factors and the relationship between testosterone dynamics and human aggression during competition

Men engage in aggression at a cost to extrinsic reward, and this behaviour is associated with a rise in testosterone. To characterize the factors underlying aggression, men were assigned to one of the four experimental conditions of a computer game in which they were provoked (points were stolen from them or not) and/or received reward for aggression (received points for aggression or not). Men who were provoked but did not receive reward for aggression enjoyed the task the most, demonstrated an increase in salivary testosterone, and were more likely to choose a competitive versus non-competitive task than men in the other experimental conditions. Moreover, individual differences in aggressive behaviour among these men were positively correlated with the extent to which they enjoyed the task and with testosterone fluctuations. These results indicate that costly aggressive behaviour is intrinsically rewarding, perhaps to regulate future interactions, and that testosterone may be a physiological marker of such reward value.

Learning and Individual differences in Aggressive Behavior Observed in Rats that Have Lived in Small Mixed Colonies

An experiment was performed to determine the relationship between open field measures (ambulation and defecation) and aggressive behavior in laboratory rats. Learning influences over this relation were considered. Colony-maintained laboratory procedure was not effective to increasethe aggresive behavior of animals when un intruder rat was placed into the colony. In the subjects not exposed to prior attack conditioning the classification variables ambulation and defecation were not enough important to determine or influence the aggression level. Nevertheless, the observed tendency was that the rats with high ambulatory scores were more aggressive than the low ones, and the rats with low defecation scores were more aggressive than the high ones. In the subjects exposed to prior attack oonditioning the Subjects with high ambulation and high defecation scores were the more aggressive. Then, these Subjects learned more quickly than the low ambulation and defecation ones.

A quantitative genetic approach to understanding aggressive behavior

AbstractQuantitative genetic studies of human aggressive behavior only partly support the claim of social role theory that individual differences in aggressive behavior are learnt rather than innate. As to its heritable component, future studies on the genetic architecture of aggressive behavior across different contexts could shed more light on the evolutionary origins of male-female versus male-male aggression.

Civilising Children: A Comment on Richard Tremblay’s “The Development of Youth Violence: An Old Story with New Data

Through a number of highly influential publications, including this one, Tremblay has challenged the ways in which criminologists, developmentalists, and prevention researchers look at violence and aggression over the life course. In a nutshell, Tremblay disputes the view, held by many criminologists that violent and aggressive behaviour starts in early adolescence and that, therefore, causes of aggression must be sought during this period of human development. In contrast, the main empirical pattern found in longitudinal studies suggests that aggressive behaviour is most prevalent between the end of the second and the end of the fourth year after birth and then becomes less frequent throughout the life course. Therefore, Tremblay argues, “we do not need to learn to aggress. We learn not to aggress. Humans and many other animal species learn to use alternatives to physical aggression”. Of course, the early propensity for aggression is not uniform. Rather, there are individual differences in aggressive behaviour at ages 2–4, some due to genetic factors, others due to environmental factors such as family dysfunction, coercive–hostile parenting, or substance use during pregnancy. But, ultimately, it is early education that matters most in civilising children, Tremblay argues along the lines of St. Augustine, Erasmus and Hobbes. If it fails, children will be at increased risk for a large number of negative outcomes, including substance use, early parenthood, unemployment, mental disorders and crime/aggression. Consequently, prevention is most effective if it focuses on quality early education. The paper by Tremblay covers a huge ground and combines a philosophical perspective on human nature, a developmental theory of aggressive and delinquent behaviour and a firm view on where we should invest in prevention. In my subsequent brief remarks, I will venture on this broad perspective and try to add some critical thoughts. Developmental Causes of Aggression: Tremblay emphasises that aggression is not learnt but that the relinquishment of violence is due to the learning of alternatives to aggression. If we accept this argument, then much of the search for risk factors of aggression is Eur J Crim Policy Res (2007) 13:171–173 DOI 10.1007/s10610-007-9051-6

Territorial aggression, circulating levels of testosterone, and brain aromatase activity in free-living pied flycatchers

Testosterone (T) is a critical endocrine factor for the activation of many aspects of reproductive behavior in vertebrates. Castration completely eliminates the display of aggressive and sexual behaviors that are restored to intact level by a treatment with exogenous T. There is usually a tight correlation between the temporal changes in plasma T and the frequency of reproductive behaviors during the annual cycle. In contrast, individual levels of behavioral activity are often not related to plasma T concentration at the peak of the reproductive season suggesting that T is available in quantities larger than necessary to activate behavior and that other factors limit the expression of behavior. There is some indication from work in rodents that individual levels of brain aromatase activity (AA) may be a key factor that limits the expression of aggressive behavior, and in agreement with this idea, many studies indicate that estrogens produced in the brain by the aromatization of T may contribute to the activation of reproductive behavior, including aggression. We investigated here in pied flycatcher ( Ficedula hypoleuca) the relationships among territorial aggression, plasma T, and brain AA at the peak of the reproductive season. In a first experiment, blood samples were collected from unpaired males holding a primary territory and, 1 or 2 days later, their aggressive behavior was quantified during standardized simulated territorial intrusions. No relationship was found between individual differences in aggressive behavior and plasma T or dihydrotestosterone levels but a significant negative correlation was observed between number of attacks and plasma corticosterone. In a second experiment, aggressive behavior was measured during a simulated territorial intrusion in 22 unpaired males holding primary territories. They were then immediately captured and AA was measured in their anterior and posterior diencephalon and in the entire telencephalon. Five males that had attracted a female (who had started egg-laying) were also studied. The paired males were less aggressive and correlatively had a lower AA in the anterior diencephalon but not in the posterior diencephalon and telencephalon than the 22 birds holding a territory before arrival of a female. In these 22 birds, a significant correlation was observed between number of attacks/min displayed during the simulated territorial intrusion and AA in the anterior diencephalon but no correlation was found between these variables in the two other brain areas. Taken together, these data indicate that the level of aggression displayed by males defending their primary territory may be limited by the activity of the preoptic aromatase, but plasma T is not playing an important role in establishing individual differences in aggression. Alternatively, it is also possible that brain AA is rapidly affected by agonistic interactions and additional work should be carried out to determine whether the correlation observed between brain AA and aggressive behavior is the result of an effect of the enzyme on behavior or vice versa. In any case, the present data show that preoptic AA can change quite rapidly during the reproductive cycle (within a few days after arrival of the female) indicating that this enzymatic activity is able to regulate rapid behavioral transitions during the reproductive cycle in this species.

Early life predictors of the development of aggressive behaviour in the domestic pig

Individuals show stable differences in their aggressive responses towards unfamiliar conspecifics. We investigated the extent to which variables present during early life could be identified that were correlated with these later individual differences in aggressive behaviour. The behaviour and growth of 125 domestic pigs, Sus scrofa, from 16 litters, were studied from birth until 18 days after weaning, when they were tested on two occasions in resident–intruder tests to measure their aggressiveness. Aggressiveness was affected by litter, although not by sex. A number of early life correlates of later resident–intruder aggressiveness were found at the litter level. Pigs became more aggressive if they had been born into larger litters. Pigs in these aggressive litters were more active in the 8-h period immediately after birth, perhaps taking longer to achieve satiety at the udder. They were also in poorer condition 2 days after birth. Aggressive pigs also engaged in more pushing with littermates over the whole preweaning period. The best correlates of aggressiveness appear to be a number of correlated variables relating to low nutrition, either prenatally or in the early postnatal period. The results are consistent with the concept that early environmental conditions can programme behavioural responses for later life.

A neural network underlying individual differences in emotion and aggression in male golden hamsters

In rodents, aggressive behavior can be altered by experimental manipulations of emotional responsiveness. The goal of this study was to identify characteristics of emotional reactivity associated with individual differences in aggressive behavior and their integration within a common neural network. Male golden hamsters were first screened for offensive aggression. Then, the animals were trained through immediate reinforcement and tested for their adaptation to a delayed reward. Similar protocols have been used to test behaviors associated with frustration. At first, all hamsters showed increased frequency of bar pressing per reward during delayed reinforcement. However, Low-Aggression animals were able to adapt to the delay and showed a decreased rate of bar pressing per reward within 5 days. In contrast, High-Aggression animals maintained a high rate of bar pressing per reward. In addition, brains were collected after immediate reward training or delayed reward testing, and labeled for pCREB-immunoreactivity as a marker of trans-synaptic activity. In High-Aggression individuals, elevated density of cyclic AMP response element binding protein, phosphorylated (pCREB) immunostaining was found within the anterior hypothalamus, an area critical to the control of aggression. Delayed reinforcement was associated with enhanced pCREB immunostaining within the central amygdala, medial amygdala and preoptic area/hypothalamus continuum. Further analysis of the data also showed a positive correlation in labeling density between the lateral septum and the anterior hypothalamus, specifically in Low-Aggression animals exposed to delayed reward. Therefore, as High-Aggression individuals lack control of their emotional reactivity, they are also characterized by a de-synchronization between the inhibitory output of the septum and the aggression areas of the hypothalamus. Finally, our data also show that frustration is associated with an extensive activation of the preoptic area/hypothalamus continuum and amygdala.

Size dominance affecting the social interactions and growth of juvenile Japanese flounder, Paralichthys olivaceus

Juvenile flounder Paralichthys olivaceus were size‐graded into three groups (small, large and mixing of small and large) and social interactions (feeding, aggressive attacking and activity) and growth of the fish were investigated. Growth of the subordinates (small flounder) was markedly suppressed by the presence of the dominants (large flounder). Dominants did not significantly suppress the overall food intake of the subordinates, but exhibited high aggressive attacking on the subordinates and consequently inhibited their activity. Size dominant interactions had little influence on the aggressive behaviour, feeding, activity and growth of the dominants. Results substantiated the hypothesis that the retardation in the growth of the subordinate flounder was attributed to the physiological costs of ‘stress’ by the aggression of the dominants. Individual differences in aggressive behaviour, feeding and activity were at least partly responsible for the growth depensation of the juvenile flounder. The dominants could not effectively defend the food in excess and disproportional food acquisition of the subordinates and dominants was not the primary mechanism responsible for the size hierarchy effect. In culture, size grading of the early juvenile flounder could markedly improve the growth and survival and thus possibly increase the overall biomass production of the flounder.

Enhanced sensitivity of postsynaptic serotonin-1A receptors in rats and mice with high trait aggression

Individual differences in aggressive behaviour have been linked to variability in central serotonergic activity, both in humans and animals. A previous experiment in mice, selectively bred for high or low levels of aggression, showed an up-regulation of postsynaptic serotonin-1A (5-HT 1A) receptors, both in receptor binding and in mRNA levels, in the aggressive line [Brain Res 736 (1996) 338]. The aim of this experiment was to study whether similar differences in 5-HT 1A receptors exist in individuals from a random-bred rat strain, varying in aggressiveness. In addition, because little is known about the functional consequences of these receptor differences, a response mediated via postsynaptic 5-HT 1A receptors (i.e., hypothermia) was studied both in the selection lines of mice and in the randomly bred rats. The difference in receptor binding, as demonstrated in mice previously, could not be shown in rats. However, both in rats and mice, the hypothermic response to the 5-HT 1A agonist alnespirone was larger in aggressive individuals. So, in the rat strain as well as in the mouse lines, there is, to a greater or lesser extent, an enhanced sensitivity of postsynaptic 5-HT 1A receptors in aggressive individuals. This could be a compensatory up-regulation induced by a lower basal 5-HT neurotransmission, which is in agreement with the serotonin deficiency hypothesis of aggression.

Human aggression and enumerative measures of immunity.

A pattern of clinical, behavioral, and experimental findings suggests that individual differences in aggressive behavior may be related to immunologic processes. We evaluated two conflicting models of the relationship: 1) A positive association stems from an adaptive mechanism protecting aggressive individuals from increased exposure to immune stimuli and 2) a negative association is due to potential immunosuppressive effects of high testosterone levels. We investigated the models using enumerative measures of cellular and humoral immunity in a sample of 4415 men aged 30 to 48 years who were interviewed and underwent a medical examination. Analysis revealed positive (and curvilinear) associations between aggressive behavior and enumerative measures of helper/inducer and suppressor/cytolytic T lymphocytes and B lymphocytes. The aggression-immunity relationship was independent of testosterone level, age, current health status, and negative health behaviors and was most pronounced for helper/inducer T cells. There was no evidence of a negative association between testosterone and any immune measure. In a large sample of men, individual differences in aggressive behavior were positively associated with enumerative measures of cellular immunity.

Children's normative beliefs about aggression and aggressive behavior.

Normative beliefs have been defined as self-regulating beliefs about the appropriateness of social behaviors. In 2 studies the authors revised their scale for assessing normative beliefs about aggression, found that it is reliable and valid for use with elementary school children, and investigated the longitudinal relation between normative beliefs about aggression and aggressive behavior in a large sample of elementary school children living in poor urban neighborhoods. Using data obtained in 2 waves of observations 1 year apart, the authors found that children tended to approve more of aggression as they grew older and that this increase appeared to be correlated with increases in aggressive behavior. More important, although individual differences in aggressive behavior predicted subsequent differences in normative beliefs in younger children, individual differences in aggressive behavior were predicted by preceding differences in normative beliefs in older children.