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PubMed2002

Frontal white matter microstructure, aggression, and impulsivity in men with schizophrenia: a preliminary study.

BACKGROUND: Aggression and impulsivity may involve altered frontal white matter. METHODS: Axial diffusion tensor images were acquired in 14 men with schizophrenia using a pulsed gradient, double spin echo, echo planar imaging method. White matter microstructural measures (fractional anisotropy and trace) were calculated from these data. Regions of interest were placed in frontal white matter on four slices. Impulsivity was measured using the Motor Impulsiveness factor of the Barratt Impulsiveness Scale. Aggressiveness was measured using the Assaultiveness scale of the Buss Durkee Hostility Inventory and the Aggression scale of the Life History of Aggression. RESULTS: Lower fractional anisotropy in right inferior frontal white matter was associated with higher motor impulsiveness. Higher trace in these regions was associated with aggressiveness. CONCLUSIONS: Inferior frontal white matter microstructure was associated with impulsivity and aggression in men with schizophrenia. These results implicate frontal lobe dysfunction in aggression and certain aspects of impulsivity.

Adult↗
PubMed2001

Aggressive behavior induced by the steroid sulfatase inhibitor COUMATE and by DHEAS in CBA/H mice.

The steroid sulfatase enzyme (STS) regulates the formation of dehydroepiandrosterone (DHEA) from dehydroepiandrosterone-sulfate (DHEAS). DHEAS is a well-known negative allosteric modulator of the GABA(A) receptor-gated chloride channels. It is classified as an excitatory neurosteroid. The implication of GABA(A) receptor activity in aggressive behavior in rodents is well-documented. In addition a genetic correlation between STS level in the liver and aggressive behavior across 12 strains of mice suggest that STS activity could be involved in aggression in mice. We assessed herein whether COUMATE (an STS inhibitor) and DHEAS modulate aggression in CBA/H mice. We hypothesized that inhibiting STS activity in vivo followed by DHEAS injections which increase the level of sulfated steroid that cross the blood-brain barrier and then modulate neurotransmitter receptors could modify the attack behavior in mice. COUMATE (10 mg/kg) was administrated p.o. alone or in combination with the neurosteroid DHEAS (0-50 mg/kg) i.p. Animals were thereafter tested for aggression. A single dose of COUMATE significantly inhibited STS activity both in the brain (70.57%) and in the liver (87%) 24 h following administration. Behavioral tests showed that the inhibitor and DHEAS enhanced aggressive behavior when animals were simultaneously subjected to both molecules. These results confirm the correlation between aggressive behavior and STS concentration in mice. In addition, we confirm that the steroid metabolism can modulate the behavior in rodents.

Aggression↗
PubMed2002

Testosterone enhances aggression of wild-type mice but not those deficient in type I 5alpha-reductase.

Testosterone's (T) aggression-enhancing effects may be mediated in part by its 5alpha-reduced, 3-hydroxysteroid dehydrogenized metabolite 5alpha-androstane-3alpha,17beta-diol (3alpha-diol). To test this hypothesis, in Expt. 1 gonadectomized (gdx) C21 mice were administered T, 3alpha-diol, or vehicle and were observed in the resident intruder test of aggression 1 h later. C21 mice administered androgens had significantly higher incidences of aggression than did vehicle-administered mice. In Expt. 2, wild-type mice and mice deficient in the 5alpha-reductase type I enzyme were administered T or vehicle and tested 1 h later in the resident intruder paradigm. Wild-type mice administered T had significantly shorter latencies and greater incidences of aggression than did 5alpha-reductase type I knockout mice administered T or vehicle-administered mice. Data from Expt. 1 are consistent with T and 3alpha-diol having similar aggression-enhancing effects, and results of Expt. 2 suggest that the inability to metabolize T to its 5alpha-reduced products may attenuate some aggression-enhancing effects of mice in the resident intruder test of aggression.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1999

Ketanserin and tetrabenazine abolish aggression in mice lacking monoamine oxidase A.

Mice deficient in monoamine oxidase A (MAO A) have elevated brain levels of 5-HT and manifest enhanced aggression. We used these mice as a model to study the role of 5-HT in aggression. Our results show that ketanserin and tetrabenazine (TBZ) strikingly abolished the aggressive behavior of MAO A-deficient mice. The anti-aggressive effect of ketanserin may be primarily mediated by 5-HT(2A) receptors. Another specific 5-HT(2A) antagonist, [R-(+)-a-(2, 3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidine-methan ol (MDL 100907), also blocks the aggression of mutant mice but was less dramatic. Ketanserin and TBZ are both antagonists of the vesicular monoamine transporter (VMAT2). The anti-aggressive effect of TBZ and part of the effect of ketanserin may be mediated by the VMAT2. Using radioligand binding and autoradiography, we also showed that the numbers of VMAT2, 5-HT(1A), 5-HT(2A) and 5-HT(2C) sites are decreased in brains of mutant mice, which may reflect down-regulation by excess 5-HT. This study suggests that ketanserin and TBZ may be developed as novel anti-aggressive agents.

Adrenergic Uptake Inhibitors↗
PubMedDate not supplied

Aggression and recent substance abuse: absence of association in psychiatric emergency room patients.

Substance abuse has been linked to aggression in community and psychiatric samples. A retrospective chart review in 311 consecutive psychiatric emergency room patients was conducted to assess the association of substance abuse and aggression in an acute psychiatric setting. Various indices of substance abuse, including positive urine toxicology for alcohol, cocaine, and/or cannabis, were not associated with aggressive behavior. Patients with positive toxicology for cocaine were less frequently aggressive than cocaine-negative patients. Among aggressive patients, the presence of psychotic symptoms was the most important factor associated with admission. These findings suggest that aggression is not a common acute manifestation of recent substance abuse in psychiatric emergency room patients. Selection factors in this population and the specifics of an acute psychiatric setting may obscure the association, if any. Acute psychosis seems to have a more important role in this setting. Future studies should focus on the prevention and early treatment of aggression in psychotic emergency room patients.

Acute Disease↗
PubMedDate not supplied

Panic-associated suicidal and aggressive ideation and behavior.

Some investigators have noted an increased incidence of suicidal ideation and attempts in individuals with panic attacks. The direct temporal relationship between the panic state and suicidal thoughts and behaviors has not been well elucidated however. Furthermore, although aggressive behavior is often manifested in individuals with suicidal behavior, the relationship between aggression and panic has received little attention. The aim of this study was to assess the frequency and type of reported suicidal and aggressive ideation and behaviors that occur during the panic state in patients with panic disorder. In order to evaluate the contribution of depression, individuals with pure (i.e. uncomplicated) panic disorder were compared with individuals who had comorbid panic and major depression. Nineteen patients with a diagnosis of pure panic disorder and 28 patients with comorbid panic plus major depression were included in the study. All patients were given the Panic, Suicide and Aggression Scale (PSAS), a questionnaire specifically designed to assess reported suicidal and aggressive thoughts and behaviors that occur during panic attacks. Other scales given to all patients included overall measures of impulsivity, suicide risk and violence risk. Patients with pure panic disorder reported high rates of suicidal and aggressive ideation and behavior during panic. The presence of comorbid depression resulted in a doubling of the rate of reported panic-associated suicidal ideation, property destruction and assaults, and a five-fold increase in the rate of homicidal ideation. The rate of reported suicide attempts was equal in the pure panic and comorbid group. There were also high correlations in all panic patients between measures of panic-associated suicide and aggression with the psychometric measures of impulsivity, suicide risk and violence risk.

Adult↗
PubMedDate not supplied

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.

Aggression↗
PubMed2002

Effects of withdrawal from anabolic androgenic steroids on aggression in adult male rats.

In gonadally intact male rats, chronic exposure to high levels of testosterone propionate (TP) increases aggression, nandrolone (ND) has little effect and stanozolol (ST) suppresses aggression. The present experiment tested whether the effects of TP, ND and ST on aggression and reproductive tissues are reversed following anabolic androgenic steroid (AAS) withdrawal. Gonadally intact males received TP, ND, ST or vehicle for 12 weeks. Injections were then discontinued. Aggression was tested 3 weeks (short term) and 12 weeks (long term) after withdrawal of AAS treatment, with either a gonadally intact or a castrated opponent in three different environments (home, opponent's and neutral cage). After short-term withdrawal, some parameters of aggression were significantly above control levels in TP males. There were no significant differences between ND or ST males and controls, though ST males showed the lowest levels of aggression. No significant differences between any of the groups were found after long-term withdrawal. Eighteen weeks after AAS withdrawal, serum testosterone (T) and LH levels were comparable to controls in all groups. Testes weights were at control levels in ST males, but significantly higher than controls in TP and ND males. Seminal vesicle weights were significantly elevated in TP males, but similar to controls in both ND and ST males. None of the prostate weights were significantly different from controls. These results suggest that aggression gradually returns to normal following withdrawal from AAS. Some, if not all, hormone levels and tissue weights return to normal, suggesting possible long-lasting effects of chronic AAS exposure.

Aggression↗
PubMed2003

Self-injurious behavior in male rhesus macaques does not reflect externally directed aggression.

Self-injurious behaviors (SIB), such as self-biting and self-wounding, have been observed in a small percentage of captive nonhuman primates. Because rhesus monkeys that exhibit SIB also tend to be more aggressive, it was hypothesized that SIB is related to externally directed aggression and is associated with contexts in which physical contact between participants is prevented. The purpose of this study was to test the hypothesized relationship between SIB and outward aggression. Subjects were first presented with videotapes of conspecifics, scenery and a blank screen, and their behavior was recorded. Levels of salivary cortisol, an indicator of stress, were also measured before and after presentation of the videos. Although aggression increased when subjects viewed tapes containing conspecifics, neither cortisol levels nor self-biting behavior varied as a function of tape content. The subjects were then placed in two additional test situations: an empty room and the same room containing an unfamiliar conspecific. Aggression was significantly higher in the stranger condition compared to the empty room condition. The two situations yielded parallel increases in cortisol, suggesting that being alone was just as stressful as being paired with an unfamiliar conspecific. Self-biting rates were also similar in these two conditions. Thus, contrary to our prediction, increases in aggression did not correlate with increases in SIB. These results suggest that under similarly stressful conditions, SIB and externally directed aggression are unrelated.

Aggression↗
PubMed2002

Central nervous system serotonergic responsivity and aggressive disposition in men.

To determine whether normative variability in aggressive behavior correlates negatively with central nervous system (CNS) serotonergic function among men, plasma prolactin (PRL) responses to a standard fenfluramine challenge (administered to assess central serotonergic responsivity) were examined in relation to interview-assessed aggression histories among 118 adult males derived from a nonpatient, community sample. Fenfluramine-induced, peak PRL rises were smaller in subjects whose 'aggression' scores fell above the sample median, compared to their less aggressive counterparts (P<.002). Across subjects, participants' peak PRL responses likewise covaried inversely with aggression history (r(s)=-.32, P<.0005). Additional analyses were conducted on data of 58 subjects who had also been genotyped for a functional polymorphism in the promoter region of the X chromosomal, monoamine oxidase-A (MAO-A) gene. The four variants of this repeat polymorphism were grouped for analysis (alleles '1+4' vs. '2+3') based on prior report of enhanced transcriptional efficiency in MAO-A promoter constructs containing alleles 2 and 3 (repeats of intermediate length). Men in the 2/3 allele group had significantly higher aggression scores (P<.05) and smaller peak PRL responses to fenfluramine (P<.009) than men in the 1/4 allele group. When adjusted by analysis of covariance for concomitant variability in subjects' PRL responses, aggressive disposition no longer varied significantly by genotype. This finding suggests that association of the MAO-A promoter polymorphism with this behavioral phenotype may be mediated, in part, by allele-specific variation in central serotonergic responsivity.

Adult↗
PubMedDate not supplied

Androgens and estrogens modulate 5-HT1A and 5-HT1B agonist effects on aggression.

Intermale offensive aggressive behavior is facilitated by gonadal steroids and inhibited by serotonin (5-HT), presumably through its effects at 5-HT1A and 5-HT1B receptor sites. To examine the interaction between these neuroendocrine and neurochemical regulatory systems, CF-1 male mice were gonadectomized and implanted with silastic capsules containing either diethylstilbestrol (DES, a synthetic estrogen), the nonaromatizable androgens methyltrienolone (R1881) or dihydrotestosterone (DHT), or testosterone (T). Two weeks later, they were given 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, a 5-HT1A agonist; 0.1 or 1.0 mg/kg), CGS12066B (a 5-HT1B agonist; 4.0 or 8.0 mg/kg), 0.1 or 1.0 mg/kg 8-OH-DPAT + 4.0 mg/kg CGS12066B, or vehicle, and tested for aggression. In the presence of DES, the higher 8-OH-DPAT dose given in combination with CGS attenuated aggression in comparison to vehicle controls. When given nonaromatizable androgen (R1881 or DHT), all drug treatments except 0.1 mg/kg 8-OH-DPAT significantly reduced offensive attack behavior. In the presence of T, which provides estrogenic and androgenic stimulation, aggression scores were significantly reduced when males were given the high dose of 8-OH-DPAT or CGS12066B, as well as in the 1.0 mg/kg 8-OH-DPAT + CGS12066B condition. Assessments of changes in motor behavior showed significant impairment when 8.0 mg/kg CGS12066B was administered across all hormonal conditions, indicating that reductions in offensive aggression in these treatment groups were nonspecific. The results demonstrate differential effects of the steroidal environment on the ability of 5-HT1A and 5-HT1B agonists to modulate aggression, with estrogens producing a more restrictive environment than androgens for serotonergic inhibition of male-typical aggressive behavior.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1981

Involvement of the GABAergic system on shock-induced aggressive behavior in two strains of mice.

The effects of drugs that antagonize or potentiate the action of brain gamma-aminobutyric acid (GABA) on shock-induced aggressive behavior in mice were investigated. In previous studies it has been shown that in C57 BL/6 strain shock-induced aggressive behavior is absent up to the 10th week of age and rises to the highest intensity after the 20th week, while at the same ages aggressive responses are lowest or absent in DBA/2 strain. GABA antagonist, picrotoxin and glutamic acid decarboxylase (GAD) inhibitor, D, L-allylglycine induced aggressive responses in non-aggressive 10 week old C57 BL/6 and 20 week old DBA/2 mice. GABA agonist muscimol hydrobromide, and GABA-T inhibitor sodium n-dipropylacetate inhibited aggressive responses in 20 week old C57 BL/6 mice. These effects were not related to changes in shock sensitivity and motor activity. The results strongly suggest that the GABAergic system is involved in the control of shock-induced aggressive behavior in mice and that this control is related to developmental and genetic factors.

4-Aminobutyrate Transaminase↗
PubMed1981

6-hydroxydopamine and aggression in cats.

The effect of 6-hydroxydopamine (6-OHDA) injected into the cerebral ventricles on behaviour of singly- and group-housed cats was investigated. 6-OHDA in doses of 0.5, 1 and 2 mg was administered every morning for 5 to 8 days. In small doses 6-OHDA in singly- and group-housed cats evoked motor phenomena such as tremor, ataxia, rigidity, weakness and sometimes clonic-tonic convulsions. Occasionally restlessness, irritability and rage were observed. Large doses of 6-OHDA in group-housed cats, after a short latent period (2-3 days) produced aggression which intensified on subsequent injections, and thereafter, on repeated administrations, no longer occurred. The aggression consisted of restlessness, irritability, anger, rage, apprehension, threat, attack, fighting, flight and crying. Of autonomic phenomena mydriasis, dyspnea and sometimes piloerection were observed. The aggression was initiated by the most restless cat, or by disturbing the animals, such as by moving the cage. When 6-OHDA no longer produced aggressive behaviour, motor changes such as tremor, ataxia, rigidity, walking on broad base, weakness with adynamia and clonic-tonic convulsions developed. These latter symptoms were produced by large doses of 6-OHDA in singly-housed cats. In these animals spontaneous signs of aggressive behaviour usually were not observed, although if handled they showed rage, snarling and hissing. When singly-housed cats were kept in the same cage with group-housed animals, the singly-housed cats usually became aggressive. It appears that hyperactivity induced aggression in 6-OHDA-treated cats.

Aggression↗
PubMed1997

Clinician's views on sexually aggressive children and their families: a theoretical exploration.

Behavioral and family characteristics of sexually aggressive children were obtained from a national convenience sample of treatment providers to gain descriptive data and to investigate the tentative use of a social learning theory model of sexual aggression of children. One hundred fifty-five professionals responded to a questionnaire of their work with a total of 287 sexually aggressive children aged 12 and under. A number of family variables may have impacted the children's sexual behavior. The average child resided in a two-parent home, and in most of these families (70%), at least one caretaker was chemically dependent; 48% have at least one parent known to have been sexually abused; and 72% of the children were sexually abused themselves (60% by a caretaker). The children with known sexual abuse histories were younger at first sign of sexual aggression than those without known sexual abuse histories. Children under 6 years of age were more likely to perceive their sexually aggressive behavior as normal than were older children. Differences based on gender of the children were not found for sexual aggression. These results suggest the potential for use of a social learning theory with sexual aggression in children. Implications for practice and suggestions for further research are discussed.

Aggression↗
PubMed1992

The aggression theory of schizophrenia: revisited.

The aggression theory of schizophrenia is a psychoanalytic theory which proposes that schizophrenia results from uncontrolled, deprivation-induced aggressive impulses. An animal model of the aggression theory is presented using predatory aggression as the source of arousal. Although neurochemical control of predatory aggression is nonspecific, anatomic control is located in the lateral hypothalamus across species. The lateral hypothalamus also controls schedule-induced polydipsia which has been implicated in schizophrenia. The aggression theory could be empirically evaluated by determining if schizophrenics respond differently than normals to scheduled feedings. Implications of the aggression theory are discussed.

Aggression↗
PubMed1988

Mice: the initiation and maintenance of pregnancy-induced aggression following thelectomy.

Two experiments were conducted in order to assess the effects of thelectomy (i.e., nipple removal) on the display of pregnancy-induced aggression in Rockland-Swiss (R-S) albino mice. Pregnant animals, thelectomized on Gestation Day (GD) 12, exhibit a high incidence and intensity of aggression toward adult R-S male intruders during tests conducted on GDs 14, 16, and 18 (i.e., during the last third of gestation in this species). Since thelectomized dams display levels of aggression (i.e., 63% incidence) equivalent to those of sham-operated and nonoperated animals (53 and 67% incidence, respectively), it would appear that nipple presence is not a critical factor for the maintenance of pregnancy-induced aggression in mice (Experiment 1). To examine the effects of nipple deprivation on the initiation of pregnancy-induced aggression, virgin animals were thelectomized prior to mating, then repeatedly tested for aggression at 2-day intervals of gestation. Unlike nipple-intact dams, pregnant mice, deprived of nipples prior to conception, rarely exhibit (less than 17% incidence) agonistic behaviors toward intruder males (Experiment 2). These findings suggest that the development and self-stimulation of nipples early in pregnancy may be important conditions for the display of heightened aggression with advancing pregnancy in mice.

Aggression↗
PubMed1997

Measurement of aggression in psychiatric patients.

This article analyzes, describes, and characterizes the methods used for measuring aggression in studies on psychiatric patients. The authors reviewed all studies published between 1985 and 1994 in seven major psychiatric journals and found 103 studies on adult aggression and 43 on childhood and adolescent aggression. Almost half (44.7%) of the adult studies and 23.3% of the child and adolescent studies did not use any structured instrument; the remainder used a total of 52 different instruments, indicating that the methodology in this area is not well established. The methods used for measuring aggression were mainly of three types: observational measures; self-report questionnaires; and structured chart reviews. Each of these tools is described herein, with special focus on reliability and validity. Overall the reliability of the various scales is high, but the empirical validity is rather poor. In choosing a suitable method for measuring aggression, researchers should take into account the direction of investigation (e.g. state vs. trait aggression, dynamic or biological aspects of aggression) and the target population. Practical suggestions in this regard are offered.

Adolescent↗
PubMed1998

Ipsapirone neuroendocrine challenge: relationship to aggression as measured in the human laboratory.

Thirty-one human subjects were administered a neuroendocrine challenge with the 5-HT1a agonist ipsapirone after completing six sessions of a laboratory measure of aggression, the Point Subtraction Aggression Paradigm (PSAP), in order to determine if a laboratory measure of aggression was related to serotonin function. Subjects who showed more aggressive responding on the PSAP (n = 11) had a significantly blunted temperature response to ipsapirone compared to those with less aggressive responding (n = 20). There was no difference between the two groups on the cortisol response to ipsapirone. This study supports a relationship between serotonin function and aggression as measured in the human laboratory, similar to the well-documented association between self-reported aggression and serotonin.

Adult↗