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Neuroendocrine responses in free-living female and male lizards after aggressive interactions.

Although female aggression is found in many species and in a variety of contexts, little is known about its physiological bases. To compare neuroendocrine responses to aggression in females and males, we staged aggressive interactions between free-living territorial mountain spiny lizards and same-sex intruders and measured brain monoamines, plasma steroid hormone levels, and plasma glucose levels. Both females and males that had participated in a staged aggressive interaction had similar changes in serotonin (5-HT) activity in telencephalic tissue punches as indicated by a lowered ratio of forebrain:brainstem 5-HT concentrations. In addition, both females and males had elevated plasma corticosterone (B) after an aggressive interaction when compared to controls. The only difference detected between males and females was that females had a higher ratio of forebrain:brainstem norepinephrine (NE) concentrations throughout the brain compared to males. Together, these data indicate that acute neural and hormonal responses that accompany aggressive interactions in females are similar to those in males.

Aggression↗

Modulation of aggression in male mice: influence of group size and cage size.

Aggression in group-housed male mice is known to be influenced by both cage size and group size. However, the interdependency of these two parameters has not been studied yet. In this study, the level of aggression in groups of three, five, or eight male BALB/c mice housed in cages with a floor size of either 80 or 125 cm(2)/animal was estimated weekly after cage cleaning for a period of 14 weeks. Furthermore, urine corticosterone levels, food and water intake, body weight, and number of wounds were measured weekly. At the end of the experiment, tyrosine hydroxylase (TH) activity, testosterone levels, and weight of spleen, thymus, testes, and seminal vesicles were determined. Results indicate a moderate increase of intermale aggression in larger cages when compared to the smaller cages. Aggression in groups of eight animals was considerably higher than in groups of three animals. The increase of agonistic behavior was observed both in dominant and subordinate animals. Physiological parameters indicate differences in stress levels between dominant and subordinate animals. It is concluded that aggressive behavior in group-housed male BALB/c mice is best prevented by housing the animals in small groups of three to five animals, while decreasing floor size per animal may be used as a temporary solution to decrease high levels of aggression in an existing social group.

Aggression↗

Exogenous testosterone, aggression, and mood in eugonadal and hypogonadal men.

To investigate (1) the effects of exogenous testosterone (T) on self- and partner-reported aggression and mood and (2) the role of trait impulsivity in the T-aggression relationship. Thirty eugonadal men with partners were randomized into two treatment groups to receive: (1) 200 mg im T enanthate weekly for 8 weeks or (2) 200 mg im sodium chloride weekly for 8 weeks. Eight hypogonadal men received 200 mg im T enanthate biweekly for 8 weeks. All groups completed a battery of behavior measures at baseline (Week 0) and at Weeks 4 and 8. Cognitive and motor impulsivity were the only predictors of self-reported total aggression (over and above age and T levels) at Weeks 0, 4, and 8. No significant changes in aggression or mood levels were found in the eugonadal-treated group. Significant reductions in negative mood (tension, anger, and fatigue) followed by an increase in vigor were found in response to T treatment in the hypogonadal group. These results demonstrate that inability to control one's behavior when such control is required by a particular situation (impulsivity) was found to significantly predict levels of aggression over and above age and T level. These data do not support the hypothesis that supraphysiological levels of T (within this range) lead to an increase in self- and partner-reported aggression or mood disturbances. Instead, for the first time, this study has identified the high level of negative affect experienced by hypogonadal patients. These findings have implications for T replacement therapy and male contraception.

Adult↗

Hypothalamic paraventricular nucleus modulates maternal aggression in rats: effects of ibotenic acid lesion and oxytocin antisense.

Central oxytocin (OT) appears to be crucial for maternal behavior. OT, through the parvocellular neurons of the hypothalamic paraventricular nucleus (PVN), can exert its physiological and behavioral effects by acting on OT receptors in nonpituitary projections of the PVN. The purpose of the present study was to analyze the role of the PVN and OT on maternal aggressive behavior in two different periods after delivery: on the fifth day (period of high aggressiveness) and on the eighteenth day postpartum (period of low aggressiveness). In the first experiment, ibotenic acid was injected into the PVN in order to lesion the parvocellular neurons. A second experiment was designed to study more specifically the effects of OT using the antisense technique. On the fifth day postpartum, both the PVN lesion by the ibotenic acid and a possible acute reduction of OT synthesis by the antisense administration in that nucleus increased maternal aggressive behavior, while on the eighteenth day postpartum no effect was recorded. We may conclude that central projections of the PVN modulate maternal aggression during a restricted period after delivery, only when lactating females show naturally high levels of aggressive behaviors.

Aggression↗

Serum estradiol levels and ethanol-induced aggression.

The biological mechanisms behind ethanol-induced aggression are not known. Because gonadal hormones are linked both to aggression and ethanol, the present study examined relationships among the levels of serum estradiol (E2), testosterone (T), and aggressive behavior in ethanol-treated male mice. We found that among group-housed male mice, serum E2 levels were significantly elevated 30 min after a single injection of 0.6 g/kg ethanol. Serum T levels showed a nonsignificant decrease by ethanol. The E2/T ratio, an index of aromatization of T to E2, was significantly higher in the ethanol-treated animals when compared with the vehicle-treated animals. We also determined aggressive behavior in the resident-intruder test among isolated male mice at baseline (after a vehicle), and after an injection of 0.6 g/kg ethanol. The mice were grouped accordingly to those that increased, decreased, or remained nonaggressive in response to ethanol administration. We found that at baseline, neither serum T or E2 levels, nor E2/T ratio differed significantly between the increased or reduced aggressor mice. In contrast to the increase in serum E2 levels seen in the nonaggressive mice, ethanol significantly reduced circulating E2 levels, but did not affect aromatization of E2 from T in the mice that became aggressive following an ethanol injection. These data suggest that mice who exhibit a paradoxical decrease in serum E2 levels by ethanol may be particularly prone to ethanol-induced aggression.

Aggression↗

Negative affect and parental aggression in child physical abuse.

OBJECTIVE: Parental negative affect is a risk factor for child physical abuse. As negative affect contributes to aggression, and because physical abuse involves an aggressive act directed at the child, we examined the relationship between negative affect and parent-to-child aggression (PTCA) in parents reported to Child Protective Services for physical abuse. METHOD: Baseline assessment data were retrospectively examined on 49 participants in a treatment study for child physical abuse. The negative affects studied were depression, anxiety, and hostility on the Beck Depression Inventory and the Brief Symptom Inventory. PTCA was assessed using the physical aggression subscales (Minor and Severe Physical Violence) of the Conflict Tactics Scale. The contribution of these negative affects to PTCA was examined after controlling individually for the effects of parental attributions and contextual variables widely regarded as etiological factors in child physical abuse. RESULTS: Contributions of negative affect to PTCA after individually controlling for other predictors were found for Minor Physical Violence but not Severe Physical Violence. Findings were strongest with depression on the Beck Depression Inventory and to a lesser extent with hostility on the Brief Symptom Inventory. CONCLUSIONS: Finding that negative affect contributed to PTCA in this sample suggests that it may be important to study the effects of emotion-focused treatments in physically abusive parents. These findings also suggest that PTCA may have qualities of impulsive aggression, a form of aggression that is conceptualized as driven by negative affect, occurs in response to aversive events, and is not planned.

Adult↗

Aggressive and social behavior after alprazolam withdrawal: experimental therapy with Ro 19-8022.

The aim of the present study was to ascertain whether withdrawal from alprazolam can increase anxiety-like and aggressive behavior during intra species conflict in mice and, if so, whether a partial benzodiazepine agonist Ro 19-8022 is able to reverse these behavioral changes without untoward effects such as sedation. An experimental model consisting of interactions of pairs of singly-housed male mice with non-aggressive group-housed male mice was used. Alprazolam (1 mg/kg) was given orally twice daily for 8 days and once on the 9th day. When withdrawn from alprazolam (3 days after the last dose), mice reduced social investigation and increased the incidence of aggressive behavior in comparison to the pre-withdrawal level. However, the increase of aggression was moderate and occurred only in subjects with low pre-treatment levels of aggression. Ro 19-8022 (10 mg/kg) significantly antagonized the decrease of social behavior and the increase of aggression after alprazolam withdrawal without causing sedation or ataxia.

Aggression↗

A double-blind placebo-controlled crossover study of phenytoin in individuals with impulsive aggression.

The present study examines the behavioral and psychophysiological effects of phenytoin (PHT) in individuals who display impulsive-aggressive outbursts. In a double-blind placebo-controlled crossover design, individuals meeting previously established criteria for impulsive aggression were administered PHT and placebo during separate 6-week conditions. The efficacy measures used were the Overt Aggression Scale (OAS) and the Profile of Mood States (POMS). Psychophysiological measures (evoked potentials) were taken at baseline and at the end of each 6-week condition. Photic stimulation was used to evoke the mid-latency P1-N1-P2 waveform complex. Analysis indicated a significant decrease in the frequency of impulsive-aggressive outbursts during PHT administration compared to baseline and placebo. Analysis of the psychophysiological data showed significantly increased P1 amplitude and significantly longer N1 latency during PHT administration. In addition, a reduction in N1 amplitude during PHT administration was also suggested. These findings indicate reparation of physiological abnormalities previously observed in impulsive-aggressive individuals and imply more efficient sensory processing and effective orienting of attention. Taken together, these results provide insight as to the physiological mechanisms by which PHT serves to ameliorate impulsive-aggressive behavior.

Adult↗

A positive correlation between self-ratings of depression and laboratory-measured aggression.

Aggression and depressive symptoms have been linked using self-rating scales as measures of aggression. In order to study this relationship using an objective measure of aggression, we studied normal controls (42 women and 23 men) with the Point Subtraction Aggression Paradigm (PSAP) and the Beck Depression Inventory (BDI). There was a significant positive correlation (r = 0.442, P = 0.003) between the level of aggressive responding on the PSAP and the level of depressive symptoms on the BDI in women but not in men (r = 0.064, P = 0.773). This study provides some evidence of a link between aggressive behavior and depressive symptoms in a non-clinical population, possibly due to a common neurochemical etiology.

Adolescent↗

Aggressive behaviour in schizophrenia: role of state versus trait factors.

The objective of this article was to elucidate the relative importance of state vs. trait factors in determining aggressive behaviour in schizophrenia. Thirty-one aggressive schizophrenia patients in rehabilitation wards were compared with 31 matched non-aggressive patients with respect to their psychopathology, phenomenologies of hallucinations and delusions, neuroleptic motor side effects, history of aggression and personality traits. Significant differences between the two groups were found in relation to psychopathology, affective responses to hallucinations/delusions, history of aggression and personality traits, but there were no significant differences regarding neuroleptic motor side effects. The effects of history of aggression as well as personality traits were independent of and similar to the total level of psychopathology, but were much smaller when compared to those of negative affective responses to hallucinations/delusions.

Adult↗

Laboratory measures of aggression and impulsivity in women with borderline personality disorder.

To characterize how severe negative affect in women is reflected in objective measures of aggression and impulsivity, the aggressive and impulsive behavior of 14 hospitalized women with borderline personality disorder (BPD) was compared with that of 17 controls. In an impulsivity task, subjects experienced two sets of 50 trials during which they could choose a smaller, immediate monetary reward or a larger but progressively delayed reward. In a separate task (PSAP), subjects earned monetary reinforcers with repeated button presses, and were provoked by the subtraction of money which was blamed on a fictitious other participant. Subjects could respond by ostensibly subtracting money from the fictitious subject (the aggressive response). While selection frequency of the short-delay responses was similar in patients and controls, BPD patients responded to avoid longer delay of reward across trials, and had higher Barratt Impulsiveness Scale total scores and attentional subscale scores. BPD patients responded to the money losses with roughly three times as many aggressive responses as controls and had higher Buss-Durkee Hostility Inventory (BDHI), Brown History of Violence, and Retrospective Overt Aggression Scale scores than controls. Aggressive responding rates correlated positively with BDHI scores. These results extend previous findings that negative affect in women is reflected in laboratory behavioral measures.

Adult↗

Influence of trait hostility on tryptophan depletion-induced laboratory aggression.

Previous research has indicated that laboratory aggression in men increases after temporarily reducing the synthesis and neurotransmission of serotonin (5-HT) in the brain using the plasma L-tryptophan (Trp) depletion technique. Further research indicates that male subjects selected for high trait hostility are particularly prone to increased aggression following plasma Trp depletion. In a recent study of laboratory aggression in male control subjects, we demonstrated that laboratory aggression increased following ingestion of a Trp-depleting beverage, but not after ingestion of a Trp-containing beverage nor under food-restricted conditions. We report here that the increases in aggression under Trp-depleted conditions were specific to men who scored the highest on the Buss-Perry Aggression Questionnaire. These preliminary data support earlier findings that compared to non-hostile men, hostile men may be more prone to behavior change induced by the perturbation of the 5-HT neurotransmitter system.

Adolescent↗

Modulatory role of 5-HT3 receptors in mediation of apomorphine-induced aggressive behaviour in male rats.

We have studied the effects of serotonin (5-HT) 5-HT3 receptor agonists 1-phenylbiguanide (1-PBG) and 1-(m-chlorophenyl)biguanide (mCPBG), and antagonists 3-tropanyl-3,5-dichlorobenzoate (MDL-72222) and tropisetron (3-tropanyl-indole-3-carboxylate HCl; ICS-205930) on apomorphine-induced aggressive behaviour in normal or DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride] pre-treated male Wistar rats. DSP-4 (50 mg/kg) pre-treatment significantly accelerated the development of apomorphine-induced aggressive behaviour. mCPBG (1.0 and 10 mg/kg) did not modify the aggressiveness, but 1-PBG (3.0 and 30 mg/kg) attenuated the aggressiveness in normal but not DSP-4 pre-treated rats. MDL-72222 (0.4 and 4.0 mg/kg) attenuated the aggressive behaviour in normal rats, tropisetron (0.3 mg/kg) had an antiaggressive effect only by citalopram (10 mg/kg) challenge. MDL-72222 and tropisetron were ineffective in DSP-4 pre-treated rats. In conclusion, our results indicate that the 5-HT3 receptors modulate the apomorphine-induced aggressive behaviour and the 5-HT3 receptor antagonists have moderate antiaggressive effect in this test.

Aggression↗

Human aggression in evolutionary psychological perspective.

This article proposes an evolutionary psychological account of human aggression. The psychological mechanisms underlying aggression are hypothesized to be context-sensitive solutions to particular adaptive problems of social living. Seven adaptive problems are proposed for which aggression might have evolved as a solution--co-opting the resources of others, defending against attack, inflicting costs on same-sex rivals, negotiating status and power hierarchies, deterring rivals from future aggression, deterring mates from sexual infidelity, and reducing resources expended on genetically unrelated children. We outline several of the contexts in which humans confront these adaptive problems and the evolutionary logic of why men are cross-culturally more violently aggressive than women in particular contexts. The article concludes with a limited review of the empirical evidence surrounding each of the seven hypothesized functions of aggression and discusses the status and limitations of the current evolutionary psychological account.

Aggression↗

Social reasoning: a source of influence on aggression.

Aggressive children show deficits and biases in their social information processing. Cognitions based on early experience and social schemas are also related to development and maintenance of aggressive behavior. Social reasoning can be linked to these aspects of social cognition, impacting on the situational cues individuals encode, their interpretations of events, and influencing response decisions. Past experience also influences development of social reasoning and social schema. Despite this, current discussion of the links between cognition and aggression rarely involves consideration of the influence of social reasoning. In this review, domain theory (E. Turiel, 1978, 1983) underpins an examination of links between social reasoning and aggression using empirical evidence drawn from research on the social reasoning of normal and aggressive children. Children as young as 3 appear to use consistent patterns of social reasoning when making judgments about transgressions and other social events, and these patterns are linked to social reasoning domains. We propose that aggressive children access information from the underlying social reasoning domains differently than their prosocial peers. This in turn affects their decision making and subsequent behavior in social situations. Our review explores developmental and clinical implications of the proposal and provides directions for future research.

Aggression↗

Preserved cerebellar tyrosine hydroxylase-immunoreactive neuronal fibers in a behaviorally aggressive subgroup of Alzheimer's disease patients.

Aggression is a very problematic behavioral symptom affecting a significant proportion of Alzheimer's disease patients. Previous work in our laboratory has shown that a subgroup of Alzheimer's patients displaying aggressive behaviors had a markedly higher level of alpha2-adrenergic receptors in the cerebellar cortex (approaching or exceeding those of controls), compared to Alzheimer's patients with similar cognitive impairments, but no history of aggressive behaviors. This study has sought to assess whether noradrenergic neuronal inputs to the cerebellum reflect similar changes in this Alzheimer's subgroup. Cerebellar cortex from non-aggressive Alzheimer's subjects showed a markedly lower level of tyrosine hydroxylase-positive neuronal fibers than normal controls (approximately 75% decreased), visualized by immunohistochemistry. Cerebellar cortex from the aggressive Alzheimer's subgroup, on the other hand, had a tyrosine hydroxylase fiber concentration not significantly different than controls. These results suggest that there is a relative preservation of inhibitory noradrenergic neuronal input to the cerebellar cortex in this aggressive subgroup of Alzheimer's disease patients. Much evidence exists that the cerebellum assists in behavioral control. The possibility that this lack of noradrenergic decline in the cerebellum could lead to a system imbalance and result in a selective behavioral disturbance is discussed.

Aged↗

Chronic anabolic-androgenic steroid treatment during adolescence increases anterior hypothalamic vasopressin and aggression in intact hamsters.

The present study examines the hypothesis that exposure to anabolic-androgenic steroids (AAS) during adolescent development predisposes hamsters to heightened levels of aggressive behavior by influencing the anterior hypothalamic-arginine vasopressin (AH-AVP) neural system. To test this, adolescent male hamsters (Mesocricetus auratus) were treated with high doses of AAS, tested for offensive aggression in the absence or presence of AH-AVP receptor antagonists, and then examined for changes in AH-AVP expression and neural organization. AAS exposure during adolescence significantly increased aggression intensity (number of attacks and bites) and initiation (latency to the first bite). Yet, only increases in aggression intensity were inhibited by AH-AVP receptor antagonism. Adolescent AAS-treated hamsters showed significant increases in AH-AVP fiber density and peptide content. However, no alterations in AH-AVP neuronal organization or mRNA expression were found. Together, these data suggest that adolescent AAS exposure increase aggression intensity by altering AH-AVP expression and activity, providing direct evidence for a causal role of AH-AVP expression and function in early onset AAS-stimulated aggression.

Aggression↗

Investigation of the relationship between farrowing environment, sex steroid concentrations and maternal aggression in gilts.

Maternal oestrogen and progesterone have been shown to be important in the initiation of maternal behaviour. Thirty-three Large White x Landrace gilts, housed in groups during pregnancy, were observed and aggressive interactions recorded. Individuals had jugular catheters implanted 14.5 (s.e. 0.34) days before their expected parturition date (EPD). Five days before EPD gilts were randomly allocated and moved to either a conventional farrowing crate (C; without straw, 16 gilts) or a pen (P; 2.1 x 3.1 m2; with straw bedding, 17 gilts). Blood samples were taken at frequencies determined by the proximity to farrowing onset. Piglets were removed at birth and returned 2 h after placental expulsion. The reaction of each gilt to her piglets was monitored. Gilts savaging piglets were sedated with azaperone (n = 8). There was no overall effect of farrowing environment on oestradiol and progesterone concentrations. The pre-farrowing ratio of progesterone to oestradiol was higher for (P) gilts (0.45 vs. 0.25, (P) vs. (C); S.E.D. 0.085, P < 0.05) as was their overall maximum oestradiol level (3.39 vs. 2.29 ng/ml, (P) vs. (C); S.E.D. 0.39, P < 0.01). In contrast to progesterone, oestradiol patterns varied considerably between individuals. Dominance rank value during pregnancy, but not levels of aggression, correlated positively to pre-farrowing oestradiol concentrations. Treatment with azaperone was not related to farrowing environment, piglet weight or litter size. Azaperone treated gilts showed a higher pre-farrowing oestradiol to progesterone ratio (0.55 vs. 0.29, +/- azaperone; S.E.D. 0.10, P < 0.05), significantly higher levels of oestradiol post-partum (0.7 vs. 0.19 ng/ml, +/- azaperone; S.E.D. 0.20, P < 0.001) and significantly lower levels of aggression during pregnancy (1.68 vs. 2.23 aggressive interactions/h, +/- azaperone; S.E.D. 0.15, P < 0.001). The results indicate that there are no major effects of farrowing environment on sex steroid concentrations. Maternal aggression under these conditions appears to be negatively related to aggression during pregnancy, but this is not reflected in plasma concentrations of sex steroids around parturition.

Aggression↗