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At least 631 records · Page 35Linked to original sources
PubMed2006

Increased accumbal dopamine during daily alcohol consumption and subsequent aggressive behavior in rats.

BACKGROUND: Alcohol drinking may lead to increased aggression in certain individuals, and both fighting and drinking increase levels of dopamine and serotonin in mesocorticolimbic structures. Assessing the dynamic changes in these neurotransmitters during the course of drinking and fighting has remained challenging. OBJECTIVE: The objective of the study was to learn about ongoing monoaminergic activity in the nucleus accumbens of rats that engaged in aggressive behavior after having consumed low doses of alcohol. MATERIALS AND METHODS: After male members of breeding pairs of Long-Evans rats displayed reliable aggression toward an intruder into their home cage, they were trained to consume a 10% alcohol solution, leading to blood alcohol levels of 20-80 mg/dl. Subsequently, the effect of daily alcohol self-administration on aggression was determined in biweekly confrontations with an intruder. Finally, rats were implanted with a microdialysis probe aimed at the n. accumbens for sample collection before, during, and after a 10-min alcohol drinking session followed by a 10-min aggressive confrontation. RESULTS: Accumbal dopamine, but not serotonin, levels tended to increase in anticipation of the daily alcohol session, reaching significance immediately after the alcohol session and remaining significantly elevated (by 40%) during and after the subsequent confrontation. No such changes were seen in residents that confronted an intruder without preceding alcohol consumption. Animals that had a history of becoming more aggressive after consumption of low levels of alcohol showed similar changes in dopamine levels as did animals that had no such history. CONCLUSIONS: The rise in accumbal dopamine confirms previous findings and seems to reflect the anticipation of alcohol consumption; it persisted during the aggressive confrontation regardless of the level of aggression. The daily alcohol drinking for several months may have facilitated dopamine release and masked any further changes associated with the aggressive encounter.

Aggression↗
PubMed1998

Alcohol-heightened aggression in mice: attenuation by 5-HT1A receptor agonists.

One of the critical mechanisms by which alcohol heightens aggression involves forebrain serotonin (5-HT) systems, possibly via actions on 5-HT1A receptors. The present experiments tested the hypothesis that activating 5-HT1A receptors by selective agonists will block the aggression-heightening effects of ethanol. Initially, the selective antagonist WAY 100635 was used to assess whether or not the changes in aggressive behavior after treatment with 8-OH-DPAT and flesinoxan result from action at the 5-HT1A receptors. Resident male CFW mice engaged in aggressive behavior (i.e. attack bites, sideways threats, tail rattle) during 5-min confrontations with a group-housed intruder male. Quantitative analysis of the behavioral repertoire revealed systematic reductions in all salient elements of aggressive behavior after treatment with 8-OH-DPAT (0.1-0.3 mg/kg, i.p.) or flesinoxan (0.1-1.0 mg/kg, i.p.). The 5-HT1A agonists also reduced motor activities such as walking, rearing and grooming, although to a lesser degree. Pretreatment with the antagonist WAY 100635 (0.1 mg/kg, i.p.) shifted the agonist dose-effect curves for behavioral effects to the right. In a further experiment, oral ethanol (1.0 g/kg, p.o.) increased the frequency of attacks in excess of 2 SD from their mean vehicle level of attacks in 19 out of 76 resident mice. Low doses of 8-OH-DPAT (0.03-0.3 mg/kg) and flesinoxan (0.1, 0.3, 0.6 mg/kg), given before the ethanol treatment, attenuated the alcohol-heightened aggression in a dose-dependent fashion. By contrast, these low 5-HT1A agonist doses affected motor activity in ethanol-treated resident mice to a lesser degree, suggesting behavioral specificity of these anti-aggressive effects. The current results support the hypothesized significant role of 5-HT1A receptors in the aggression-heightening effects of alcohol. If these effects are in fact due to action at somatodendritic 5-HT1A autoreceptors, then the anti-aggressive effects would be associated with decreased 5-HT neurotransmission.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1999

The effects of tryptophan depletion and loading on laboratory aggression in men: time course and a food-restricted control.

Some studies have shown that sharp reduction of L-tryptophan (Trp) concentration in plasma results in increases in laboratory-measured aggression. Conversely, raising plasma Trp has blunted aggression. These effects are presumably due to impaired or enhanced serotonin synthesis and neurotransmission in the brain. In this study, the laboratory-measured aggressive behavior of eight men under both Trp depletion (T-) and Trp loading (T+) conditions was compared to their aggressive behavior under food-restricted control conditions (overnight fast without an amino acid beverage). Subjects were provoked by periodic subtraction of money which was attributed to a fictitious other participant, and aggression was defined as the number of retaliatory responses the subject made ostensibly to reduce the earnings of the (fictitious) other participant. Following ingestion of the T- beverage, aggressive responding was significantly elevated relative to the food-restricted control condition, and this increased aggressive behavior became more pronounced across behavioral testing sessions on a time-course which paralleled previously documented decreases in plasma Trp concentrations. In contrast, no changes were observed in aggressive responding under T+ conditions relative to food-restricted conditions. These within-subject behavioral changes under depleted plasma Trp conditions support earlier indications of a role of serotonin in regulating aggression.

Adult↗
PubMed2006

Genes and developmental stabiltiy of aggressive behavior problems at home and school in a community sample of twins aged 7-12.

Though behavioral genetic studies of aggression have implicated heritable and environmental factors, there is limited understanding of how these factors influence aggression across different settings and over time. Ratings for 732 twins were collected from parents and teachers during middle childhood and early adolescence. Total aggression scores on the Child Behavioral Checklist (CBCL) and Teacher Report Form (TRF) were examined at each age, across both settings, and developmentally. In this sample, aggressive behavior was moderately to largely heritable at each age within the home (.76-.84) and school (.42-.61). Across each age, ratings by parents and teachers were moderately correlated (.19-.36). Genetic and environmental effects that were limited to a particular setting were important etiological factors for aggressive behavior consistently within each setting, while only genetic factors influenced levels of aggression across both settings. Stability during these ages was due to genetic effects common to each age and the persistence of child-specific environmental experiences within each setting. These results suggest that genetic and environmental influences on children's aggressive behavior are largely setting specific. Levels of aggression seen consistently across both settings are due to genetic influences. Developmentally stable levels of aggressive behavior result from genetic influences common to all ages and individual environmental influences whose effects persist across ages.

Aggression↗
PubMed2005

Trajectories of peer-nominated aggression: risk status, predictors and outcomes.

Developmental trajectories of peer-nominated aggression, risk factors at baseline, and outcomes were studied. Peer nominations of aggression were obtained annually from grades 1 to 3. Three developmental trajectories were identified: an early-onset/increasers trajectory with high levels of peer-nominated aggression at elementary school entry and increasing levels throughout follow-up; a moderate-persistent trajectory of aggression in which children were characterized by moderate levels of physical aggression at baseline; and a third trajectory with stable low levels of aggression. Children following the early-onset/increasers trajectory showed physical forms of aggression at baseline. Male gender and comorbid attention deficit/hyperactivity problems, oppositional defiant problems and poor prosocial behavior plus negative life events predicted which children would follow the early-onset/increasers trajectory of aggression. The outcomes associated with the early-onset/increaser children suggest high risk for chronically high levels of aggressive behavior.

Aggression↗
PubMed1996

Relationship of prolactin response to d-fenfluramine to behavioral and questionnaire assessments of aggression in personality-disordered men.

Prolactin (PRL) responses to acute challenge with the serotonin (5-HT) releaser/uptake inhibitor, d-fenfluramine (PRL[d-FEN]), were correlated with three different measures of aggression in 14 male personality-disordered subjects. Consistent with previous work, PRL[d-FEN] responses were inversely correlated with scores on the Buss-Durkee Hostility Inventory-Assault scale (BDHI-Assault) and with the Brown-Goodwin Aggression-Revised (BGA-R) Aggression scale. In addition, PRL[d-FEN] responses were inversely correlated with a direct laboratory measure of aggressive behavior (Point-Subtraction Aggression Paradigm: PSAP). Although all measures of aggression correlated with PRL[d-FEN] response, differences among the intercorrelations of these measures were found. Specifically, BGA-R Aggression scores correlated with both BDHI-Assault and PSAP scores, but no relation was found between BDHI-Assault and PSAP scores. The results suggest that central 5-HT function may be associated with both self-report and behavioral measures of aggressive behavior, which may represent somewhat separate aspects of aggressive behavior.

Adult↗
PubMed1989

Activation of mu opioid receptors in the nucleus raphe dorsalis blocks apomorphine-induced aggression in rats: serotonin appears not to be involved.

The role of mu opioid receptors in the nucleus raphe dorsalis (DR) in the control of apomorphine-induced aggression was studied in rats. Administration in the DR of a selective mu opioid receptor agonist, (D-Ala2,N-Me-Phe4,Gly5-ol)-enkephalin (DAGO), in doses ranging from 0.01 to 1 microgram/0.5 microliter, dose-dependently reduced aggression caused by apomorphine 20 mg/kg intraperitoneally. 0.01 microgram DAGO significantly reduced the time spent by the animals in aggressive posture and 0.1 and 1 microgram markedly reduced both aggressive postures and attacks. 5 micrograms (in 0.5 microliter) naloxone in the DR completely antagonized the anti-aggressive effect of DAGO (0.1 microgram/0.5 microliter) injected in the same area. 0.1 and 1 microgram but not 0.01 microgram DAGO significantly increased serotonin (5-HT) metabolism in the striatum, a terminal area almost exclusively innervated by DR, indicating that the activity of 5-HT cells in the DR was modified by DAGO. In animals given 6 micrograms/3 microliters 5,7-dihydroxytryptamine in the DR 11 days before, in which striatal 5-HT levels were markedly depleted, no significant changes were found in the time spent by the apomorphine-treated animals in aggressive postures, numbers of attacks or anti-aggressive effect of 0.1 and 1 microgram DAGO administered in the DR. The study shows for the first time that activation of mu opioid receptors in the DR has a powerful anti-aggressive effect in one model of experimental aggression by a mechanism apparently not involving changes in the activity of 5-HT cells in this area.

Aggression↗
PubMed1988

Testosterone control of territorial behavior: tonic-release implants fully restore seasonal and short-term aggressive responses in free-living castrated lizards.

Two aspects of hormonal control of aggressive territorial behavior in male mountain spiny lizards Sceloporus jarrovi were studied. First, testosterone (T) implants were given to free-living castrated males during the breeding season. These implants fully restored breeding season levels of aggressive and sexual behavior. Earlier studies showed that identical implants given to free-living males during the nonbreeding season did not induce full breeding season levels of aggression. The full effectiveness of these implants during the breeding season indicates that the lack of effectiveness in the nonbreeding season was not due (1) to the need to replace additional gonadal factors or (2) to ineffectiveness of tonic delivery by the implants. It is more likely that males are less sensitive to T during the nonbreeding season or that other cues present in the breeding season environment synergize with T to induce full levels of aggression. Thus, seasonal changes in aggressive behavior in male S. jarrovi cannot be explained simply as a direct response to changes in circulating levels of T; other environmental factors play a necessary role as well. In the second phase of the study, changes in aggressive behavior of free-living T-implanted castrates were monitored following staged encounters with other males. Despite their inability to alter secretion rates of T, the T-implanted castrates still showed a rapid postencounter increase in aggressive displays that was identical to controls. Previous results showed that this dramatic postencounter increase in aggressive behavior is not accompanied by simultaneous changes in circulating T. Together, these results now allow the hypothesis that this rapid behavioral change in aggressive behavior is caused by simultaneous changes in circulating T levels to be confidently rejected.

Aggression↗
PubMed1990

Aromatization mediates aggressive behavior in quail.

Although testosterone (T) stimulates aggressive and reproductive behaviors in males of many vertebrate species, it is now known that the full expression of T action in the brain requires aromatization to estradiol (E2) and subsequent interaction of locally formed E2 with nuclear estrogen receptors. In experiments reported here, we used a behavioral test which quantifies the response of an individual male Japanese quail (Coturnix coturnix japonica) to the visual stimulus of a conspecific. We have called this behavior aggression because it shares many features in common with traditional measures of aggression, e.g., predicting dominance and subordinance. Nevertheless, the behavior probably also combines a complex steroid-sensitive masculine behavior. The advantage of this test is that it allows the discrimination of individual differences in masculine behavior but avoids fighting and sexual encounters per se, thereby reducing effects of learning, a problem with previous tests of avian aggression. In addition, this test has been applied usefully to identify neuroendocrine correlates to male behavior. Using this test, the arousal of reproductively inactive males (hereafter referred to as aggression) is activated by administration of T or estradiol benzoate (EB), but not by 5 alpha-dihydrotestosterone (DHT). T-induced aggression was blocked by the aromatase inhibitor 4-hydroxyandrostenedione (OHA), an effect partially reversed by treatment with EB. In addition, OHA or the estrogen receptor blocker CI-628 reduced aggressiveness of reproductively active males whereas the androgen receptor blocker flutamide had no effect. Results with the 5 alpha-reductase inhibitor N,N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane-17 alpha-carboxyamide (4-MA) were equivocal. Additionally, treatment of reproductively inactive quail with T or E2 but not DHT increased aromatase activity in the hypothalamus-preoptic area (HPOA). We conclude, therefore, that T to E2 conversion is essential for the activation of aggressiveness in this species. Although locally formed estrogen exerts its effects on aggression in part by increasing activity of aromatase per se, analysis of the time course of behavioral induction or suppression by the various treatments suggests that the response has multiple components, including both short latency, receptor-independent and long latency, receptor-dependent events.

5-alpha Reductase Inhibitors↗
PubMed1984

The role of progesterone in pregnancy-induced aggression in mice.

A series of six experiments was performed in order to explore the potential involvement of progesterone (P) in pregnancy-induced aggression (PIA) displayed by Rockland-Swiss mice toward adult male intruders. In Experiment 1, circulating levels of P and aggression were low on gestation Days 6 and 10 while both the behavior and the steroid reached peak levels by gestation Day 14. By gestation Day 18 (the day prior to parturition), serum P was at its lowest level yet aggressive behavior was still intense. Also, individual differences in the display of fighting behavior by pregnant females were not related to circulating P. Experiments 2 and 3 showed that supplemental P treatment to early pregnant female mice did not advance the onset of aggression. Experiment 4 showed that P treatment promoted the onset and elevated the incidence of aggression in virgin mice, but only in those females with intact ovaries. Experiment 5 showed that the aggressive behavior of P-stimulated virgin females was qualitatively and quantitatively different from that exhibited by pregnant mice in that the former exhibited fewer attacks and lunges than the latter. Finally, Experiment 6 showed that the removal of P from aggressive, P-stimulated virgins dramatically attenuated levels of the behavior. This contrasts sharply with the continued fighting behavior observed in late pregnant P-deficient mice. Thus, although P augments aggression in female mice it apparently is not a sufficient stimulus for producing pregnancy-like aggressive behavior.

Aggression↗
PubMed1986

Sex-specific interactions between aggressive and sexual behavior in the rat: effects of testosterone and progesterone.

The influence of progesterone on sexual and aggressive behaviors during aggressive encounters was investigated in pairs of TP-treated male and female rats. Gonadectomized females, chronically injected with testosterone propionate (TP), showed low but consistent levels of feminine sexual behavior which alternated with aggression. Progesterone when given in addition to TP facilitated receptive and proceptive behaviors, but reduced levels of aggression. In TP-treated males, levels of aggression were the same as observed in TP-treated females. However, TP-treated males seldomly showed sexual behavior during aggressive encounters and additional treatment with progesterone did not affect their behavior. After the aggression tests, animals were tested in a social preference test in which an ovariectomized female cage mate and the opponent from the aggressive encounter served as incentives. Positive correlations between levels of aggression and social preference for an opponent were found in both sexes, although correlations only reached statistical significance when progesterone was given in addition to TP. These correlations were found in both sexes, despite the fact that group analysis revealed pronounced sex differences in social preference: males preferred to spend their time near ovariectomized female cage mates, whereas females divided their time equally among female cage mates and opponents.

Aggression↗
PubMed1991

Types of aggressiveness and catecholamine response in essential hypertensives and healthy controls.

Relationships between plasma catecholamine responses, and levels and types of aggression in hyper- and normotensives were investigated by analyses of data obtained in a large psychophysiological experiment on 97 hypertensives (EH) and 98 normotensives (CO) each. Subjects were divided according to levels (high vs low) and types (repressed vs manifest) of aggressiveness according to self rating questionnaire scores. Their plasma catecholamine responses to defined stressors indicating sympathetic arousability were compared by four factor analyses of covariance adjusting for age. Repressed aggression was significantly more frequent among male EH, whereas manifest aggression was significantly more frequent among the male COs. High as compared to low hostility was associated with significantly elevated values of plasma epinephrine in EH but not in CO. The immediate norepinephrine stress response was blunted but showed a delayed increase during the subsequent period of rest in high aggressives of both the EH and CO group, a pattern particularly pronounced in repressed aggressive hypertensives. Neither cardiovascular reactions nor speed of performance were observed to be substantially different in subjects of repressed and of manifest hostility. It was concluded that aggression in general is characterized by a delayed norepinephrine stress response and that an association with high epinephrine is typical for aggressiveness in hypertensives. Repressed hostility, however, does not produce a sympathomedullary pattern substantially different from that of manifest aggression thus casting doubt on the physiological significance of repression claimed by Alexander.

Aggression↗
PubMed1984

Effects of mother-litter separation and reunion on maternal aggression and pup mortality in lactating hamsters.

This study examined the effects of a 24 hr mother-litter separation on maternal aggression and pup mortality in hamsters. There were four lactating groups tested for aggression in their home cages on days 5 and 15 postpartum: a group that was separated from their litters for 24 hr, a group that was not separated from their litters and two 24 hr separation groups in which the litters were returned 30 and 120 min prior to the aggression test. Nonreceptive, estrous cycling animals were used as controls (tested twice, 10 days apart) and as intruders. Measures of aggression recorded during the 10 min tests included the number of attacks, fights, chases and intruder retreats. Pup mortality was examined in the 4 lactating groups and in two additional non-tested groups, one of which was separated from their litters for 24 hr. Lactating hamsters initiated significantly higher levels of aggression than control animals. Mother-litter separation (24 hr) significantly decreased levels of aggression and these levels were restored when litters were replaced 30 and 120 min prior to aggression tests. There were few differences in levels of aggression between days 5 and 15 of lactation. Pup mortality was significantly greater between days 5-6 and 15-16 of lactation among those groups that were separated from their litters compared to those groups that were not separated. Significantly higher mortality levels were found between days 7 and 15 of lactation among the 2 groups in which pups were returned prior to the aggression test compared to all other groups.

Aggression↗
PubMed1988

Cohabitation with a female activates testosterone-dependent social aggression in male rats independently of changes in serum testosterone concentration.

Male hooded rats (350 to 450 g) were sham-castrated, castrated and implanted with testosterone-filled, or castrated and implanted with empty Silastic tubes. Twenty-four hours postoperatively the animals in each group were housed with a female or a male similar in size to the female. Beginning one week following surgery and continuing for three weeks thereafter, the female or male cagemate was removed once each week while a 15-min test of aggression toward an unfamiliar male intruder was conducted. During the aggression tests, lateral attacks, lunge attacks, bites, on-top, and piloerection were recorded. At the first aggression test, males housed with females were significantly more aggressive than their counterparts housed with males. In contrast, different testosterone regimes did not consistently influence the initial activation of intermale social aggression. At the second and third tests, males with testicular testosterone or a replacement were significantly more aggressive than their castrated controls on most measures but males housed with females continued to be more aggressive than the comparable group housed with males. These results suggest that normal fluctuations in serum testosterone concentration associated with sexual interaction are not necessary for the initial activation of intermale social aggression. Both repeated exposure to unfamiliar males as well as cohabitation with a female are effective stimuli for activation of testosterone-dependent social aggression.

Aggression↗
PubMed1993

Influence of combined estradiol and testosterone implants on the aggressiveness of nonaggressive female rats.

Female rats that had been cohabiting with a sterile male or with another female for 6 weeks were tested for aggression toward an unfamiliar female once each week for 3 weeks. Females that were not aggressive as a result of cohabitation with a sterile male were ovariectomized. Half were implanted with a Silastic tube containing estradiol (1 mm long hormone-filled space) and a tube containing testosterone (5 mm long hormone-filled space). The other half were implanted with empty tubes. All females that had been cohabiting with another female were ovariectomized and implanted with an estradiol- and a testosterone-filled tube. Three additional weekly tests of aggression were given beginning 1 week postoperatively. Females given hormone replacement displayed only a slight increase in aggression postoperatively. Females not given hormone replacement declined in aggressiveness. These results indicate that hormone replacement levels sufficient to maintain aggression in highly aggressive females following ovariectomy are not sufficient to produce a high level of aggression in females that have not become aggressive following cohabitation with a sterile male or that have been cohabiting with another female.

Aggression↗
PubMed1989

Effects of d-amphetamine on human aggressive responding maintained by avoidance of provocation.

Male subjects were administered placebo and three doses of d-amphetamine (5, 10 and 20 mg per 70 kg of body weight) under double-blind conditions in a laboratory setting which provided both aggressive and nonaggressive response options. the nonaggressive response was button pressing maintained by the presentation of points which were exchanged for money. The aggressive response was pressing another button which ostensibly resulted in the subtraction of points from a fictitious person. Aggressive responding was initiated by subtracting points from the subject. Point subtractions were attributed to the other person. Aggressive responding was maintained by an avoidance contingency between aggressive responses and scheduled provoking point subtraction presentations. d-Amphetamine increased nonaggressive responding, while aggressive responding was increased at the 10 mg dose and 20 mg resulted in significant decreases in aggressive responding relative to the 10 mg dose. Comparisons with previous research indicate that the contingency relationship between aggressive responses and presentation of provoking point subtractions can alter the effects of d-amphetamine on aggressive responding.

Adolescent↗
PubMed1983

Ethological analysis of drug action on aggression and defense.

Psychopharmacological research on aggression pursues divergent objectives: From a pharmacological perspectives, animal aggression tests are employed in order to differentiate classes of psychotherapeutic drugs and to screen for specific agents. Psychiatric interests in animal aggression research attempt to model pathological aggressive behavior in humans. These efforts have yielded disappointing results because they are based neither on a detailed understanding of the behavioral characteristics of aggression nor of the relevant neural processes. The ethological approach to aggression research focuses on biologically relevant situations and behavior patterns. Quantitative methods describe drug action on the interactive and episodic nature of aggressive behavior. An analysis of the temporal pattern of aggressive behavior indicates how, for example, amphetamine and alcohol modulate sequences of aggressive interactions.

Aggression↗
PubMed1996

The influence of fluoxetine on aggressive behavior.

A large body of evidence from studies in humans, in nonhuman primates, and in smaller laboratory animals has supported a role for serotonin in the modulation of aggressive behavior. The evidence shows that diminished serotonergic function can be linked to aggressive behavior and that treatments that increase serotonergic function reduce aggression. Embedded in this large body of data are studies done specifically with fluoxetine, a serotonin uptake-inhibiting antidepressant drug suggested by some individuals charged with criminal aggression and by their attorneys to cause aggressive violence. Contrary to those charges, extensive studies of fluoxetine in animals have shown that fluoxetine decreases aggressive behavior in various species and models of aggression. Clinical studies of fluoxetine in aggressive behavior have been more limited, but findings in those studies seem consistent with the anti-aggressive effects of fluoxetine found in animal studies.

Aggression↗