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Desensitization to portrayals of real-life aggression as a function of exposure to television violence.

In two separate experiments, the hypothesis that exposure to violence in the context of television drama decreases subjects' emotional responsivity to portrayals of real-life aggression was tested. Subjects were shown either an excerpt from a violent police drama or a segment of an exciting but nonviolent volley-ball game before watching a videotaped scene of real aggression. Emotionality was measured by changes in skin resistance which was measured continuously throughout the session. In Experiment 1, subjects were 8- to 10-year-old children and the real aggression was a film of an argument and fight between two preschoolers. In Experiment 2, college students participated and reactions to real aggression were measured while subjects watched scenes from news films of the riots at the 1968 Democratic National Convention. With the exception of adult females, subjects who previously had viewed the aggression drama were less aroused by the scenes of real aggression than were subjects who had seen the control film. Further support for the hypothesis was provided by the finding that for most groups of subjects, the amount of television violence normally viewed was negatively related to responsivity while viewing aggression.

Adult↗

[Clopheline-induced aggression in mice: role of genotype and the dopaminergic system].

Clophelin (CLO) in a dose 10 mg/kg induced aggressive behaviour in mice significantly dependent of genotype. Pretreatment with flupentixol and haloperidol inhibited or blocked CLO-evoked aggression in high-aggressive mice. Apomorphine administered with CLO enhanced aggression in low-aggressive mice. Stimulation of D2 receptors by bromocriptine failed to change CLO-induced aggression. It was suggested that dopamine system was involved in CLO-aggression through D1 receptors.

Aggression↗

[Effects of muscimol on aggressive behaviors induced by clonidine in mice].

A behavioral study was carried out to clarify a relationship between the GABAergic and purinergic central system in aggressive behaviors induced by clonidine in mice. Mice administered a high dose of clonidine (20 mg/kg, i.p.) exhibited aggressive behaviors such as biting and attacking. These behaviors are inhibited by L-PIA (N6-L-phenylisopropyl adenosine) and stimulated by caffeine, which suggest that a blockade of adenosine receptors is involved in these behaviors. Muscimol (0.5-2 mg/kg, i.p.), a GABA-a receptor agonist, not only markedly potentiated clonidine (20 mg/kg i.p.)-induced aggressive behaviors but also elicited characteristic behaviors such as gnawing, reinforced irritability, and self-mutilation. Bicuculline (1, 2 mg/kg, i.p.), a GABA-a receptor antagonist, or picrotoxin (1 mg/kg, i.p.), a chloride channel blocker, did not significantly affect clonidine (20 mg/kg, i.p.)-induced aggressive behaviors. The potentiating effects of muscimol (0.5, 1 mg/kg, i.p.) on clonidine-induced aggressive behaviors were antagonized by bicuculline (1, 2 mg/kg, i.p.), but not affected significantly by picrotoxin (1 mg/kg, i.p.). L-PIA (0.2 mg/kg, i.p.) reduced clonidine-induced aggressive behaviors and also reversed the potentiating effects of muscimol. Stereotyped gnawing behaviors induced by combined treatment of muscimol (0.5, 1 mg/kg, i.p.) and clonidine (20 mg/kg, i.p.) were not affected by bicuculline (2 mg/kg, i.p.). The results suggest that the potentiating effects of muscimol on clonidine-induced aggressive behaviors may be induced via the stimulation of GABA-a receptors, although not necessarily associated with chloride channel functions, and may involve certain interactions between the stimulation of GABA-a receptors and the inhibition of adenosine receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Aggression↗

GABAergic agents and clonidine attenuate footshock-induced aggression in mice.

The effects of gamma aminobutyric acid (GABA), baclofen, and clonidine was studied on footshock-induced aggression in mice. A lower dose (200 mg/kg) of GABA enhanced the aggressive score, while at a higher dose (400 mg/kg) it attenuated the aggressive behavior, the latter effect being reversed both by bicuculline and picrotoxin (PTX). Clonidine (0.5 and 1 mg/kg) enhanced the aggressive score, and the effect of clonidine was reversed by idazoxan. GABA (400 mg/kg) and clonidine (1 mg/kg) significantly reduced the aggressive score in reserpinized mice. Baclofen (5 mg/kg) showed no effect per se in either reserpinized or non-reserpinized mice. On concomitant administration of clonidine (0.5 mg/kg) with a subeffective dose of either GABA, baclofen, or diazepam, there was significant reduction in the aggressive score. A modulatory role of GABAergic and noradrenergic systems in footshock-induced aggression is suggested.

Aggression↗

Can aggressive behavior in humans be modified by beta blockers?

Persistent aggressive behavior may develop in patients with brain disorders of various types, including seizure disorders, mental retardation, metabolic disorders, head injury, and in some instances schizophrenia. Although a neurochemical basis for aggression in these cases is unclear, a hyperadrenergic state is considered to be one possibility. This has led to the hypothesis that beta blockers may be useful in the control of aggression. The original assumption was that the site of antiaggressive action of beta blockers is in the brain. However, the antiaggressive efficacy of nadolol, which does not cross the blood-brain barrier to any great extent, suggests a peripheral site or sites. A review of several studies in which both old and young aggressive patients with various organic brain disorders received propranolol showed that aggressive behavior was reduced in 75 (86%) of 87. These results are encouraging because none of the patients had responded to earlier drug treatment. However, with the exception of one study of nine patients, none of the studies were controlled for placebo effects and most were retrospective. Preliminary results suggest tentative guidelines for treatment of aggressive behavior with beta blockers. Further studies are needed, and these should use a prospective, longitudinal double-blind design; large enough patient samples to permit testing hypotheses about disease-specific or symptom-specific responses to beta blockers; and improved instruments for measuring and classifying aggression.

Adolescent↗

[Pharmacological treatment of syndromes of aggressivity].

In the treatment of violent-aggressive behavior, four major groups of drugs emerged: 1. Major tranquilizers in the treatment of aggressive-violent behavior associated with psychotic syndromes. 2. Anti-epileptic drugs such as diphenylhydantoin and barbiturates in the treatment of aggressive-violent behavior within the epileptic syndrome. 3. Psychostimulants in the treatment of aggressive behavior of adolescents and children within behavior disturbances. 4. Anti-male hormones such as cyproterone acetate in the treatment of violent-aggressive behavior associated with pathological sexual hyperactivity. Whereas each category of drug is predominantly effective in one type of aggressive syndrome, it may also be effective in other conditions as well. Aggression as a result of a personality disorder is most difficult to treat with drugs.

Aggression↗

[The personality and self-concept of aggressive children: a typologic approach].

A sample of 57 children aged 9 to 14 years with aggressive behavior disorders was compared with an unselected clinical control group of non-aggressive children with regard to personality traits and child psychiatric classifications. The children were divided into groups of more or less aggressive symptoms (mainly aggressive--partly aggressive--non aggressive patients) and after statistical grouping according to personality traits. Three type factors could be extracted, and their relationship to the principal symptoms was analyzed. Finally the relevance of the three type factors for an efficient classification and therapy of children with aggressive conduct disorders is discussed.

Adolescent↗

Sensory control of maternal aggression in Rattus norvegicus.

Female rats become aggressive toward adult conspecifics during lactation. This change in social affect is dependent on the presence of the offspring, because maternal aggression disappears when the pups are removed. It was found that a similar decline occurs when the litter is placed in a glass flask while remaining in the home cage. In contrast, maternal aggression persists following placement of the pups in a nylon mesh bag. The pups did not vocalize while being in the mesh bags, so it appears that olfactory cues from the offspring constitute a critical element in the maintenance of maternal aggression in the rat. It has been suggested that the odor not only of the pups but also of the intruder may contribute to eliciting aggressive behavior in lactating rodents. In line with this proposal, it was found that mother rats spend about one third of the time preceding the first attack sniffing the body of the intruder. In contrast to findings in mice, housing of the prospective intruder behind a double wire mesh partition in the lactating female's home cage failed to reduce her aggressiveness toward him. Rats, then, may require more intimate contact with an individual than do mice for the aggression-reducing effect of familiarization to be observed.

Aggression↗

[Is pain-induced aggression actually a defensive form of that behavior?].

25-minute testing of aggressive reactions in constant pairs of male rats, elicited by electric shocks shows that electro-pain aggression of rats is not a homogeneous process, but consists of three successive stages: orienting-investigatory activity and attempts to get out of the chamber; defensive aggression; establishing of relations of domination-subordination and attacking aggression. Division in attacking rats and defending themselves, occurs mainly at final stages of testing (15-25 min); in some pairs reactions of attacking aggression are accomplished by the same rats. It is supposed that rats pain aggression is not a purely defensive form of this behaviour, but a modification of intermale aggression caused by specificity of laboratory conditions.

Aggression↗

The social learning of aggression in youth football in the United States.

Our investigation was designed to examine a) the extent to which young male football players and nonplayers learned about illegal aggressive actions through the observation of college and professional football; b) if there was a relationship between youth football players' observations of illegal aggressive acts and the transmission of those acts to players' own games; and c) if there were differences between high school players' and youth league players' awareness of illegal aggressive acts and the use of those acts in their games. The volunteer subjects were 347 high school football players and 122 high school nonplayers between the ages of 15 and 18 years, and 125 youth league football players and 133 junior high or middle school nonplayers between the ages of 12 and 14 years. Results revealed that players consumed significantly more college and professional football than nonplayers. Although statistically significant, players learned, through observation, only one more illegal aggressive act on the average than nonplayers. High school players learned an average of only 1.4 more aggressive acts than youth league players. Results also revealed significant correlations between the number of illegal aggressive acts that players observed and the number of those acts used in their own games for both high school (r = .62) and youth league (r = .50) players. It appears that many illegal aggressive acts are observed through college and professional football by young football players and nonplayers and a relationship exists between the observation of illegal acts and their subsequent use in players' games.

Adolescent↗

Effect of prepubertal versus postpubertal castration on sexual and aggressive behavior in male horses.

Males horses castrated prepubertally occasionally display stallion-like sexual and aggressive behavior as adults. A retrospective survey of 140 horse owners was undertaken to compare the effectiveness of prepubertal versus postpubertal castration on objectionable sexual and aggressive behavior. Of 94 geldings that had been castrated prepubertally (before 2 years of age), 20% to 30% displayed stallion-like sexual behavior and aggression toward horses, and 5% were aggressive toward people in a stallion-like manner. This occurrence of problem behavior was not significantly different from the occurrence of these behavioral patterns in 46 geldings that had been castrated as stallions (over 3 years of age). When castration was examined as a therapeutic measure to eliminate sexual and aggressive behavior in stallions in which the behavior had become objectionable, it was found that the operation was effective on sexual behavior and aggression toward people in 60% to 70% of horses and on aggression toward horses in 40% of horses.

Aggression↗

Determination of the role of serotonergic and cholinergic systems in apomorphine--induced aggressiveness in rats.

Aggressive behavior was produced in rats by administration of apomorphine (APO) 20 mg/kg ip. Serotonin (5-HT) agonists, L-tryptophan or 5-hydroxytryptophan and a MAO inhibitor, pargyline, suppressed the APO-induced aggressiveness. However, cyproheptadine was the only one of four 5-HT antagonists used which potentiated the aggressive behavior. Cyproheptadine, metergoline and PCPA released aggressiveness in rats pretreated with a subthreshold dose of APO. Cholinomimetics (pilocarpine, oxytremorine and physostigmine) completely blocked APO induced aggressiveness while cholinolytics (atropine and scopolamine) partially suppressed the inhibiting effect of pilocarpine on aggressive behavior. The results obtained suggest the existence of an interaction between serotonergic, cholinergic systems and dopaminergic system in apomorphine-induced aggressiveness in rats.

Aggression↗

[Role of serotonin2 receptors in regulating aggressive behavior].

Quipazine and pirenperone , the drugs interacting with serotonin2 -receptors, more readily displaced 3H-spiroperidol from its binding sites in the frontal cortex than in the striatum. Pirenperone (0,07-0,3 mg/kg), antagonist of serotonin2 -receptors, selectively decreased the intensity of apomorphine aggressiveness. The antiaggressive action of haloperidol (0,01-0,2 mg/kg) was in correlation with its antistereotypic activity. Long-term administration of naloxone (0,5; 15,0 mg/kg), together with apomorphine (0,5 mg/kg) reduced the number of head-twitches caused by quipazine (2,5 mg/kg). The administration of quipazine 48 hours after the last injection of naloxone and apomorphine caused spontaneous aggressiveness that did not differ from apomorphine aggressiveness. Intracerebroventricular injection of cholecystokinin tetrapeptide (CCK-4) markedly enhanced the foot-shock aggression. The same dose of CCK-4 also decreased the intensity of quipazine (2,5 mg/kg) head-twitches. Compared to haloperidol, pirenperone was a more selective antagonist of CCK-4. After long-term apomorphine treatment (0,5 mg/kg during 10 days, twice daily), the effect of CCK-4 on aggressive behaviour was markedly enhanced. It is possible that two subtypes of serotonin2 -receptors exist in the brain and have opposite action on the aggressive behaviour. CCK-4 may play the role of an endogenous modulator of sensitivity of serotonin2 -receptors involved in the control of aggressiveness.

Aggression↗

The importance of central nicotinic receptors in footshock-induced aggression in mice.

The action of nicotine and other agonists of central cholinergic receptors on aggressiveness was tested in the footshock-induced fighting test in mice. Nicotine in doses 0.25-2 mg/kg ip and 5-30 micrograms ivtr potentiated the aggressiveness, but a dose of 4 mg/kg ip suppressed it in naive (not pretested) mice. Of other cholinergic agonists betanechol, a specific muscarinic agonist, facilitated the aggression. Similar effect was produced by arecoline, a muscarinic-nicotinic agonist, while carbachol, a compound of pharmacological profile similar to that of arecoline, was ineffective. Mecamylamine, a central nicotinic antagonist, in doses 2 and 4 mg/kg moderately facilitated the aggressiveness, while in a dose of 8 mg/kg inhibited it. Hexamethonium, a peripheral nicotinic antagonist, strongly potentiated aggressiveness. Mecamylamine and hexamethonium antagonized the facilitatory action of nicotine on aggression in non-pretested mice, and of arecoline both in non-pretested an pretested mice, but did not change the effect of betanechol. The results indicate that in addition to muscarinic receptors, the nicotinic receptors in the central nervous system may participate in evoking affective aggression in mice subjected to electric foot-shock.

Aggression↗

On the biological basis of sex differences in aggression.

The prevalence of aggression as a predominantly male behavior pattern has often been noted. The nature and perceived extent of sex differences in aggression have recently revived interest in speculation that such differences are attributable to factors inherent in the biological basis of sex differentiation. This paper will critically examine the empirical and theoretical basis for Maccoby and Jacklin's contention that males are biologically predisposed toward aggressive behavior. The literature to be examined includes: (1) cross-cultural studies of children's behavior, (2) the behavior of nonhuman primates, (3) sex hormones and aggression, and (4) early learning influences in child development. Contrary to Maccoby and Jacklin's assertions, these first 3 research traditions are found to indicate no biological predisposition toward aggression in human males. Furthermore, the pattern of existing evidence suggests that the gender-dimorphic nature of aggression is reliably observable in children's spontaneous behavior only after the age of 5 years. This finding presents great difficulty for the biological theory as proposed by Maccoby and Jacklin. Suggestions are presented for an interactional theory of the etiology of observed sex differences in adult aggression.

Aggression↗

[Animal models of aggression and serotonin receptor subtypes].

Aggressive behavior is an intrinsic behavior of most animals. A number of animal models of aggression have been used to evaluate the effectiveness of anxiolytics and antidepressants in the preclinical trials. These models interested investigators in search of the mechanism of presentation of aggression. Over the past decade, serotonin (5-hydroxytryptamine, 5-HT) receptor subtypes have been identified. Various serotonergic agents have been tested, and some of them successfully reduced aggressive behavior in animal models of aggression. These include 5-HT1A receptor agonists. In the present review, after a description of various animal models of aggression is given, authors overview the role of serotonergic mechanism in the CNS and discuss its relation to aggressive behaviors.

Aggression↗

[Violent and aggressive behavior among patients in emergency wards].

The purpose of this investigation was to identify risk factors for violent and aggressive behaviour in patients in the Emergency Room (ER) with a view to suggesting prophylactic measures. From 1st December 1991 to 30th November 1992 all staff at the biggest ER in Denmark (Odense University Hospital) who had felt themselves exposed to aggressive or violent behaviour from patients answered a questionnaire about the incident. There were 47,013 contacts to the ER and 36 incidents involving violence or aggression towards hospital staff during the study period, corresponding to an incidence of 1/1306 patient contacts (0.08%), or one episode every ten days. In no cases did the violence result in staff injury requiring medical treatment, and there was only one case of dangerous violence (an aggressive patient threatened staff with a knife). The police were called in to assist in 50% of cases. Most (83%) of the incidents were caused by men. Seventy-five percent of the aggressive patients (including all six aggressive women) were easy to identify because they were visibly under the influence of either alcohol, narcotics of medications. Incidents occurred most commonly in the evenings, particularly weekends and holidays, which could possibly be associated with the general increase in alcohol consumption at these times. Long waiting-times were involved in 22% of the cases, and it is therefore proposed that waiting-times should be shortened by organizational changes. Review of the literature reveals that aggressive and assaultive behaviour is multifactorial, caused by a combination of personal and situational factors. Provoking factors in the ER environment are rarely recognized.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

A comparison of aggressive-rejected and nonaggressive-rejected children's interpretations of self-directed and other-directed rejection.

The hypothesis that aggressive-rejected children are unaware of their social status because they are self-protective when processing negative peer feedback was tested in 3 studies. In Study 1, fourth-grade girls and boys were asked to name peers they liked or disliked, as well as peers they thought liked or disliked them. Comparisons of aggressive-rejected, nonaggressive-rejected, and average status groups revealed that aggressive-rejected children were more unrealistic in their assessments of their social status than were nonaggressive-rejected children. In Study 2, rejected and average boys identified in Study 1 were asked to name who they thought liked or disliked other children from their classroom. Comparisons of perceived and actual nominations for peers revealed that aggressive-rejected children were able to assess the social status of others as well as did nonaggressive-rejected and average status children. Because the difficulties aggressive-rejected children demonstrated in Study 1 did not generalize to judging the status of others in Study 2, the self-protective hypothesis was supported. Study 3 provided a parallel test of this hypothesis under more controlled conditions. Subjects from Study 2 viewed other children receiving rejection feedback from peers in videotaped interactions and received similar feedback themselves from experimental confederates. While all subjects rated self-directed feedback somewhat more positively than other-directed feedback, aggressive-rejected subjects had the largest self-favoring discrepancy between their judgments of self- and other-directed feedback. These findings also suggest that aggressive-rejected children may make self-protective "errors" when judging other children's negative feelings about them. Ethnicity differences in evaluating peer feedback emerged in Studies 1 and 3, raising questions about the impact of minority status on children's evaluations of rejection feedback.

Aggression↗