Aggressive behavior induced by electrical stimulation in the midbrain central gray of male rats

Electrical stimulation via electrodes implanted in the lateral hypothalamus may induce intraspecific aggressive behavior. Small electrolytic lesions placed via these electrodes resulted in a five– to tenfold increase in the current threshold for aggression. Degenerating fibers were stained by means of the Fink-Heimer method and could be followed caudally to the dorsal midbrain central gray and to the mammillary bodies. A few axons could be traced rostrally to the medial septum. Aggression could be induced from 10 of 112 electrodes implanted in the central gray; the other electrodes elicited either locomotion, vocalization, jump, or “alarm-like reactions.” The morphology of the induced aggression was similar to the morphology of the hypothalamically induced aggression, though it was often accompanied with motor disturbances and was less intense. Hypothalamic stimulation was combined with simultaneous central gray stimulation in rats with electrodes both in the hypothalamus and in the central gray. Hypothalamic thresholds for aggression could be lowered by this stimulation of the central gray, even when no aggressive responses were observed during central gray stimulation alone. This suggests that, although aggression is not manifest, electrical stimulation may activate neural tissue involved in aggressive behavior. It is concluded that in rats central gray and hypothalamus are part of the same neural network mediating intraspecific aggression.     

Effects of midbrain central gray lesions on spontaneous and electrically induced aggression in the rat

Large electrolytic lesions were placed in the midbrain central gray of male rats. Their effects on hypothalamically induced aggression, switch-off behaviour, and locomotion were investigated. A number of these animals were also tested for territorial intermale aggression in order to compare electrically induced and spontaneous aggression. Large lesions resulted in an increase of the current threshold to induce aggression by hypo-thalamic stimulation. Smaller, but still quite large, lesions decreased the threshold current for hypothalamic aggression. After the operation a decrease in the threshold for switch-off was present, both in the experimental and the control group. Current thresholds for locomotion were decreased after the lesions only in the experimental group. Spontaneous aggression was temporarily decreased after the lesion. No indication was found that other behavioural elements of the animal were distorted by the lesion. The parallel between the effects on spontaneous and electrically induced aggression makes it attractive to ascribe a role to the neural circuit of hypothalamus and central gray in territorial aggression. However, even with large lesions the animals were still capable of fighting, hence the central gray is not indispensable. An attempt was made to explain the differential effects that differently sized central gray lesions have on hypothalamic aggression.     

Gender differences in the negative affective priming of aggressive behavior

The negative affective priming of aggression was examined across different aversive contexts (general stress exposure and frustration) with a laboratory aggression paradigm that measured the intensity of shocks participants delivered to a putative employee. Participants' emotional responses were gauged via startle eyeblink reactions and self-report mood ratings. Aside from gender differences in overall aggression, men but not women exposed to general stress showed significant increases in aggression across blocks. However, frustration produced increases in aggression in both genders. Although both genders showed robust startle increases during stress, startle activation was related to increases in aggression in men and decreases in aggression in women. These findings suggest that general stress and experiences of negative emotion trigger physical aggressive responses more strongly in men than in women.     

Internalizing Symptoms and Affective Reactivity in Relation to the Severity of Aggression in Clinically Referred,Behavior-Disordered Children

We examined the affective correlates of aggression in children referred to a partial hospitalization program for the treatment of behavior disorders who did not have a mood or anxiety disorder. Parent and teacher ratings of the children’s impulsivity, internalizing symptoms, affective reactivity, and aggression were examined for their interrelationships and then entered into regression analyses to predict the child’s level of aggression in the home, at school, and in the treatment program. Intercorrelations among three affective reactivity factors were modest. Both internalizing symptoms and affective reactivity contributed to aggression severity beyond impulsivity and demographics. Only child irritability predicted treatment program aggression. Because of their potential role in understanding children’s behavioral disturbances, internalizing symptoms and negative emotionality merit careful assessment and treatment in treatment programs serving hard-to-manage children with behavior disorders.     

运用赌博任务测查不同攻击/受欺类别儿童的情感决策过程

攻击行为认知研究存在的一个重要问题是忽视情感对儿童认知加工的影响。考虑了情绪－认知整合过程的儿童行为决策更能全面而真实地反映社会信息加工情境下的攻击/受欺行为卷入过程。情感决策的赌博任务范式被认为能诱发类似于个人真实生活决策的表现,本研究运用计算机程序编制的标准赌博任务,以过程的视角考察了不同攻击/受欺儿童的情感决策特点。结果发现,不同类型儿童的有利-不利选择净分数、对有利-不利选择及奖惩频数的决策偏向存在显著差异。研究结果反映未卷入儿童在赌博任务上的整体表现优于其他类型儿童,攻击-受欺儿童仅次于未卷入儿童;直接攻击、攻击-受欺、未卷入儿童呈现惩罚定向的决策风格,但这三类儿童也表现出截然不同的趋势。     

Midbrain-hypothalamic interrelationships in the control of aggressive behavior

Previous studies have suggested an involvement of the midbrain ventral tegmental area in the biting attack upon a rat elicited by electrical stimulation of the lateral hypothalamus in cats. In order assess further the relationship between these two regions, 12 cats were implanted with attack-eliciting electrodes in both the lateral hypothalamus and the midbrain ventral tegmental area. Following a lesion of the midbrain attack site, attack previously elicited from hypothalamic electrodes ipsilateral to the lesion was eliminated or significantly reduced in frequency. The attack elicited from electrodes in the hypothalamus contralateral to the lesion was unaffected. Midbrain lesions made at sites from which attack was never elicited had no effect on hypothalamically elicited attack. The midbrain lesion in some cases eliminated only certain components of the total attack pattern; for example, the approach of a cat to the rat frequently remained present while the bite was absent. Additionally, it was found that the attack elicited from rostral hypothalamic electrodes was disrupted to a greater degree by a single midbrain lesion than the attack elicited from more caudal hypothalamic electrodes. These finding are discussed in terms of the neural system mediating this form of aggressive behavior in cats.     

The role of affective and cognitive empathy in physical, verbal, and indirect aggression of a Singaporean sample of boys

Bullying behavior is a serious form of school violence, affecting many children. This study investigated the contributions of 2 specific components of empathy (affective and cognitive empathy) on the 3 forms of aggressive behaviors in a sample of 241 Grade 4 and Grade 5 boys from Singapore. The 2 components of empathy differed in their relation with the 3 types of aggression. After accounting for cognitive empathy, affective empathy was associated with physical aggression. Neither affective empathy nor cognitive empathy was associated with verbal aggression. With control for affective empathy, cognitive empathy was associated with indirect aggression. Results suggest that empathy training based on specific deficits may be helpful in intervention and prevention of specific aggressive behaviors.     

Reactivity and aggression in the rat: induction by alpha-adrenergic blocking agents injected ventral to anterior septum but not into lateral septum.

Intracranial injections were made bilaterally through permanently implanted cannulas ending in the lateral septum or in the region ventral to the anterior septum. The rats were first screened with injections of a local anesthetic, lidocaine, which blocks both synaptic and axonal conduction. Those animals that showed an increase in reactivity and aggression were then injected with a synaptic transmitter blocking agent. The results showed that transmitter blocking agents reproduced the effect of the local anesthetic only in the region ventral to the anterior septum and that alpha-adrenergic (phentolamine, tolazoline), but not beta-adrenergic (propranolol, hydralazine), cholinergic (atropine, hyocine), or dopaminergic (haloperidol) blocking agents were effective. These results suggest that synapses in the forebrain system controlling reactivity and aggression are alpha-asrenergic and are located in the region ventral to the anterior septum just lateral to the diagonal band of Broca. The septum itself may be involved only to the extent that it is traversed by fibers of passage.     

Differential Associations Between Psychopathy Dimensions,Types of Aggression,and Response Inhibition

Findings on executive functioning in psychopathy are inconsistent. Different associations between psychopathy dimensions and executive functioning might explain contradicting findings. This study examined the role of psychopathy dimensions and types of aggression in response inhibition among 117 male adolescents (53 antisocial delinquents and 64 controls). Participants completed a self‐report measure of aggression and a GoNoGo task. Psychopathy dimensions were assessed using the Psychopathy Checklist: Youth Version. Although high scores on the antisocial dimension and reactive aggression were associated with poor response inhibition, the affective–interpersonal dimension, proactive aggression, and verbal intelligence (IQ) were related to better response inhibition (two‐factor model). Associations with the affective–interpersonal dimensions did not reach significance. Exploratory analyses showed that affective and antisocial facets accounted for the obtained opposing associations of the affective–interpersonal and antisocial psychopathy dimensions with response inhibition. The interpersonal and lifestyle facets (four‐facet model) were unrelated to response inhibition. Results could not be explained by Attention Deficit Hyperactivity Disorder (ADHD). Findings suggest differential associations between the psychopathy dimensions, types of aggression, and response inhibition. Therefore, a dimensional approach to psychopathy and related concepts, such as aggression, might strongly improve diagnostic procedures. Global scores could mask important differential associations. Aggr. Behav. 38:77‐88, 2012. © 2011 Wiley Periodicals, Inc.     

Are the interpersonal and identity disturbances in the borderline personality disorder criteria linked to the traits of affective instability and impulsivity?

This study examines the degree to which two putative biologically influenced personality traits, affective instability and impulsive aggression, are associated with some of the interpersonal and intrapsychic disturbances of borderline personality disorder (BPD) and with choice of defense mechanism. In a sample of 152 personality disorder patients, affective instability and impulsive aggression were measured. Defense mechanisms were assessed in 140 of these patients using the Defensive Style Questionnaire (DSQ). The correlations between the traits of affective instability and impulsive aggression and the eight DSM-III-R criteria for borderline personality disorder and 20 DSQ defenses were examined. Affective instability was significantly correlated with the DSM-III-R criteria of identity disturbance, chronic emptiness or boredom, inappropriate anger, suicidality, and the affective instability criteria. It also was associated with the defenses of splitting, projection, acting out, passive aggression, undoing, and autistic fantasy. Impulsive aggression was related to unstable interpersonal relationships, inappropriate anger and impulsiveness and with the defense of acting out. It was negatively correlated with the defenses of suppression and reaction formation. A number of the interpersonal and experiential disturbances and defense mechanisms that are features of BPD are associated with the traits of affective instability and impulsive aggression among patients with personality disorders.     

Affective predictors of preschoolers' aggression and peer acceptance: direct and indirect effects

Observational assessments were made of 51 preschoolers' (mean age = 53.25 months) peer aggression and emotional displays outside of (baseline) and during aggressive interactions, and their emotion knowledge and peer acceptance were also assessed. Results indicated that the connections between children's affective dispositions and their aggression and peer acceptance varied as a function of both the emotion context (baseline vs. aggression related) and the particular emotion involved (happiness vs. anger). Emotion knowledge and affective dispositions overlapped little with each other, and both made independent contributions to peer acceptance and aggression. Mediation analyses revealed, however, that the significant connections between children's emotional dispositions and knowledge and their peer acceptance were mostly mediated by aggression.     

The Comprehensive Resource Model®: Overview of basic affects in adversity & effective treatment for complex reactions to trauma

Much of the theoretical focus in post‐traumatic stress disorder has been on the role of the amygdala, the hippocampus and the prefrontal cortex. Crucially, in unresolved traumatic experiences that underlie clinical presentations, this focus misses the brain areas key to the defence responses of fight, flight and freeze—and the associated affects of anger, fear and grief. The periaqueductal gray in the midbrain, with the hypothalamus, is essential for these somatic and emotional responses to traumatic experiences. We argue that when treatment approaches thought to work at the higher brain levels have been ineffective, it is because they have failed to engage the midbrain and hypothalamic sources of the affective responses to the trauma and to the memory of it. Basic affects have been so overwhelming that dissociation, or a similarly protective neurochemical capping mechanism, has prevented full resolution of the affective content of the adversity. Treatment with the Comprehensive Resource Model^® (CRM) aims to clear the clinically relevant residues of adverse experiences by resolving the emotional responses accessed through the body memories. When the trauma has led to overwhelming distress, and/or dissociation, there is a necessity for robust resourcing to be in place before the emotional intensity of that distress is accessed. Resourcing needs to be as proximal to the re‐experience as possible to promote complete resolution and in some psychotherapy modalities, the supports provided are somewhat remote from the crucial moments of processing. Therefore, we describe how the CRM seeks to have robustly resourced states present concurrently with traumatised states to avoid overwhelming emotional distress. This allows safe entry into the deepest pain residual from the traumatic event so that it is not overwhelming during processing of the memory, and does not lead to further dissociation, allowing the individual to remain fully present throughout. This “stepping into the affect” can then be so rapidly effective that we also argue that CRM is not an exposure treatment; re‐orientation to the deepest content of the experience resolves the residual distress quickly and permanently through memory reconsolidation. Re‐learning at upper brain levels will then follow from the revoking of the affective power, which has previously driven stimulus/context and response learning in the amygdala, hippocampus and prefrontal cortex.     

Stress exposure and affective modulation of aggressive behavior in men and women

To study differences in the effects of stress exposure and affective responding on aggression in men and women, the authors examined the effects of an acute stressor (air blast) on subsequent aggressive behavior, measured as the intensity of shocks men and women delivered to a putative employee. The authors measured participants' affective responding using the startle reflex. Results showed that although men and women did not differ in their startle responses to the actual stressor, high stress led to contrasting patterns of subsequent aggressive behavior. Women under high stress responded with less aggression than women under low stress, whereas men exposed to high stress exhibited increases in aggression relative to those under low stress. Affective responding during the stressor differentially modulated aggression in men and women: Startle responses predicted increasing levels of aggression in men and less aggression in women. These findings suggest that although men and women show similar basic affective processing in response to stressors, the behavioral profiles associated with stress differ in men and women. These findings have implications for understanding gender differences in the prevalence of internalizing and externalizing psychopathology.     

Cool and hot executive function as predictors of aggression in early childhood: Differentiating between the function and form of aggression

Executive function (EF) has been implicated in childhood aggression. Understanding of the role of EF in aggression has been hindered, however, by the lack of research taking into account the function and form of aggression and the almost exclusive focus on cool EF. This study examined the role of cool and hot EF in teacher reported aggression, differentiating between reactive and proactive as well as physical and relational aggression. Children (N = 106) completed laboratory tasks measuring cool (inhibition, planning, working memory) and hot EF (affective decision‐making, delay of gratification). Cool, but not hot, EF significantly contributed to understanding of childhood aggression. Inhibition was a central predictor of childhood aggression. Planning and working memory, in contrast, were significant independent predictors of proactive relational aggression only. Added to this, prosocial behaviour moderated the relationship between working memory and reactive relational aggression. This study therefore suggests that cool EF, particularly inhibition, is associated with childhood aggression across the different functions and forms.     

Depression as a risk marker for aggression: A critical review

Depression is commonly thought of as counter-indicative of aggression because of apparent contradictions in energy requirements and blame orientation. However, empirical studies indicate that the presence of depression elevates risk for general aggression, intimate partner aggression, and self-aggression. Most of these studies are cross-sectional and retrospective, hence, there is scant empirical evidence for depression as a causal factor for aggression. However, there is considerable evidence for an association between depression and aggression. Depression as a risk marker for aggression may stem from a third factor such as genetics, personality disorder or insecure attachment. There are also a number of sequelae of depression that may contribute to this increased risk for aggression including isolation, lost social support, increased alcohol use, angry rumination, and impulsivity. Furthermore, affective swamping clouds attributional clarity so that internal and external attributions for negative feelings become fused and undifferentiated. Hence, negative events of sufficient affective impact can generate both depression and anger. One form of this affective swamping is scapegoating: finding an external person or persons to blame for “causing” aversive affect. For these reasons, depression should constitute a routine aspect of mental health assessment and where present, should be viewed as a risk factor for aggression.     

The relationship between impulsive verbal aggression and intermittent explosive disorder

Intermittent explosive disorder (IED) is the sole psychiatric diagnostic category for which aggression is a cardinal symptom. IED focuses on physical aggression, but researchers have argued for the inclusion of verbal aggression (VA) (e.g., arguing, threatening) as a part of the IED criteria set. The utility of VA in identifying clinically relevant aggression, however, is unknown. IED participants were compared to individuals without a marked history of physical aggression, but who report frequent (two or more times a week) VA, and non-aggressive personality-disorder individuals on behavioral and self-report measures of aggression, self-report measures of related constructs (e.g., anger, affective lability), and a clinician assessment of psychosocial impairment. Both the IED and VA groups were more aggressive, angry, and clinically impaired than personality-disorder individuals, while the IED and VA groups did not differ from each other on these measures. These results support the clinical importance of frequent VA for future iterations of the IED criteria set.     

Defense reaction elicited by microinjection of kainic acid into the medial hypothalamus of the rat: antagonism by a GABAA receptor agonist.

Electrical stimulation of either the midbrain central gray or the medial hypothalamus induces a defense reaction in the rat, characterized mainly by increased locomotion, rearing, and leaping. However, microinjection of the excitatory amino acid glutamate was effective only in the former region. Because excitatory amino acids do not depolarize axons of passage, it was suggested that the hypothalamus is devoid of soma/dendrites of neurons commanding the defense reaction. In the present study, we show that a subtoxic dose (60 pmol) of another excitatory amino acid, kainic acid, injected into the medial hypothalamus significantly enhanced locomotion and rearing of Wistar rats systematically observed in an open field. Similar behavioral changes have been reported following microinjection of drugs impairing GABAergic neurotransmission. Local pretreatment with the GABAA receptor agonist THIP (2 nmol) blocked the effect of kainic acid. Therefore, the medial hypothalamus of the rat seems to contain a population of neuronal cell bodies commanding the defense reaction, which is activated by excitatory amino acids and tonically inhibited by GABAergic fibers.     

Bidirectional associations between affective empathy and proactive and reactive aggression

Preliminary evidence indicates that affective empathy is differentially related to proactive and reactive functions of aggression. However, additional longitudinal research is needed to understand the potential reciprocal nature of these links. The current study examined the bidirectional associations between affective empathy and proactive and reactive aggression over a 6-month period during middle childhood, with attention to potential gender differences. Data were collected from 294 elementary school children (52% girls; M = 9.25 years; SD = 0.944 years) and their homeroom teachers. Affective empathy was assessed using self-reports, and teachers provided ratings of children's functions of aggression. Data were collected during the fall and spring of one academic year. Overall, results suggest some evidence that affective empathy and functions of aggression are reciprocally linked over time. As predicted, Time 1 empathy was inversely associated with Time 2 proactive aggression and Time 1 reactive aggression was inversely associated with Time 2 empathy. Contrary to expectations, Time 1 proactive aggression was marginally positively associated with Time 2 empathy, and Time 1 empathy was not significantly associated with Time 2 reactive aggression. These prospective links did not differ according to gender. Implications and directions for future research are discussed.     

Errors of commission and omission: comment on Anderson and Anderson's (1998) "temperature and aggression"

This note identifies errors in a review of research on heat and aggression by Anderson and Anderson (1998), and it reaffirms a previously stated conclusion: Violence in a midwestern city, in 1987 and 1988, can be explained more parsimoniously and completely in terms of routine activity theory than by Anderson and Anderson's general affective model of aggression.     

Shame and aggression: Theoretical considerations

Within the shame literature, anger and aggression are widely recognized as responses to shame. Recent findings on the affective neuroscience of social pain suggest multiple models by which social pain (e.g., shame) and anger/aggression may be linked. These models describe the mechanisms underlying the prominent role of shame in interpersonal aggression, a role revealed by many dozens of studies. Anger and aggression in response to shame may be viewed as emotion regulation, coping strategies, and evolutionary adaptations. Unfortunately, these attempts at coping with shame may be adaptive or maladaptive. Indeed, aggression may be an adaptive defensive response to physical pain and many physical threats that, through evolutionary processes, came to be linked to shame once social pain co-opted the affective response to physical pain. In a related article (Velotti, Elison, & Garofalo, 2014), we review the many contexts and populations in which aggression manifests, providing further evidence for the models proposed here. Thus, a more complete understanding of anger and violent behavior requires consideration of social pain, shame, and shame-regulation, for which physical pain serves as a useful model.