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PubMed1984

Postweaning social experience and adult aggression in rats.

One group of male rats was reared continuously in small, stable colonies of three animals each during a ten-week period beginning when they were 46 days old. A second group of animals was also reared in small groups of three animals each but membership within these colonies was randomly changed at weekly intervals. Thereafter, all subjects were housed in individual cages. A 24 hr test of the subjects' aggression toward an unfamiliar male conspecific at 130-133 days of age indicated that only the heaviest animal in each of the stable colonies was aggressive. In contrast, all animals in the random-composition group were aggressive toward intruders. Scores on a second test of intruder-directed aggression administered when the subjects were nine months old were significantly related to scores on the first aggression test. Subtle variations in social experience during development are critical in establishing long-term patterns of aggression toward conspecifics in laboratory rats.

Aggression↗
PubMed1987

A method to quantify aggressiveness in Japanese quail (Coturnix c. japonica).

Testing procedures which rely on paired fights are unsuitable for measuring individual aggressiveness because the outcome of initial encounters influences subsequent dominance status. In an effort to circumvent this problem, we developed a test system which quantifies aggressiveness in individual Japanese quail by measuring locomotor and pecking activity of test birds presented with the visual stimulus of a conspecific. Using this procedure, we demonstrate that aggression is specific to sexually mature males; however, the intensity of the behavior varies widely among individuals. Scores for each bird are constant with time, reproducible, independent of the gender or behavior of the stimulus bird and accurately predict the outcome of a subsequent paired fight. In addition, we show that fighting per se produces increases and decreases in aggressiveness of dominant and subordinate birds, respectively, and re-orders the rank of a group of birds. This test procedure, therefore, confirms earlier studies which indicate that dominance hierarchies are influenced by initial encounters. Finally, repeat testing is reliable and gives an absolute, not relative, measure of aggressiveness. We conclude that this behavioral test can be applied to future studies addressing the social, developmental and endocrine basis of aggressiveness and dominance in quail and other vertebrates.

Aggression↗
PubMed1987

Effects of repeated as compared to single aggressive confrontation on nociception and defense behavior in C57BL/6 and DBA/2 mice.

Behavioral reactions (submissive postures, escape, immobility, activity, locomotion) in C57BL/6 and DBA/2 test mice were recorded during single (50 bites) or three repeated (3 X 50 bites, separated by 24 hr) aggressive confrontations, as well as during a nonaggressive confrontation 24 hr after the last aggressive confrontation with opponents of the opposite strain. Nociception (hot plate response latency) was measured 1 min after aggressive or nonaggressive confrontations. During repeated aggressive confrontation, DBA mice reacted with a stable pattern of escape and analgesia, whereas C57 mice failed to develop an analgesic response and changed their behavioral defense strategy during repeated aggressive confrontations (decrease of escape, increase of defensive upright). The conditioned display of submission and of escape behavior during nonaggressive confrontation did not change as a function of earlier repeated aggressive confrontations in DBA mice, while C57 mice showed a significant increase of defensive upright postures and immobility. Conditioned analgesia was not observed after nonaggressive confrontations. The results point toward a dissociation between attack-elicited behavior and antinociception and suggest that encounter-induced analgesia may influence the processing of aversive experience.

Aggression↗
PubMed1987

Intermale social aggression in rats: suppression by medial hypothalamic lesions independently of enhanced defensiveness or decreased testicular testosterone.

Medial hypothalamic lesions or sham lesions were made in castrated adult male rats with subcutaneous implants of testosterone-filled silastic capsules. Seven days following surgery all animals were given a test of defensiveness (reactivity) toward an experimenter. The following day, groups composed of one lesioned male rat, one sham-lesioned male rat, and one intact female rat were placed in large cages. Beginning two weeks later, unfamiliar intruders were introduced into each colony on a weekly basis and the aggressive behavior of the residents recorded. All 12 of the sham-lesioned animals but only 2 of 12 lesioned animals displayed substantial intermale social aggression toward intruders. Analysis of individual elements of intermale social aggression indicated that the lesioned animals were deficient in attack, bite, and piloerection but not in on-top behavior. The deficit in intermale social aggression was not correlated with defensiveness toward the experimenter or body weight of the lesioned animals. It is argued that the medial hypothalamus plays a role in the modulation of intermale social aggression which is independent of its role in modulating defensiveness or testosterone production. These results also demonstrate that intermale social aggression develops even when testosterone levels are held relatively constant by replacing testicular testosterone with an artificial testosterone source.

Aggression↗
PubMed1992

Differential effects of neonatal testosterone treatment on aggression in two selection lines of mice.

Selection lines of mice, artificially selected for aggression based upon the attack latency score (ALS), were used. In order to determine the relative contribution of neonatal testosterone (T) in the development of aggression, we vary the plasma-T level in males of both selection lines on the day of birth. At 14 weeks the ALS was measured. Neonatal T treatment results in a reduction of aggression in the long attack latency (LAL) line, whereas aggressive behaviour of the short attack latency (SAL) line is not affected. Both selection lines show reduction in testicular weight, although the total amount of T-producing Leydig cells was not affected. Neonatal T may cause a permanent reduction in aggressive behaviour in in the LAL line only, probably due to differential appearance of critical periods. It is suggested that the difference in aggressive behaviour between SAL and LAL selection lines is due to a prenatally determined difference in neonatal T sensitivity of the brain.

Aggression↗
PubMed1994

Influence of the mother on development of aggressive behavior in male rats.

The present experiments investigated pre- and postnatal maternal effects on aggressive behavior in rats. Resident-intruder aggressive behavior of male rats in colonies (two males and two females) was studied in five experimental groups: 1 = WWY (n = 7) the two males of each colony were wild (biological father and mother were wild) fostered by a wild mother; 2 = WAY (n = 11) the two males were wild fostered by an albino Wistar mother; 3 = AAY (n = 11) the two males were albino (biological father and mother were Wistar) fostered by an albino mother; 4 = AWY (n = 12) the two males were albino fostered by a wild mother; and 5 = HWX+HAX (n = 9) one of the males was hybrid born and reared by a wild mother (the father was albino) and the other was also hybrid but born and reared by an albino mother (the father was wild). Each test lasted 10 min and the intruder was always a Wistar male. Aggression of wild rats was higher than the laboratory ones, independently of the mother (albino or wild) they were fostered by. However, hybrid males born and reared by a wild mother were more aggressive than those that were born and reared by an albino mother, in spite of the father being wild. In conclusion, crossfostering has little effect on territorial aggression, but prenatal maternal effects seem to play a major role on the ontogeny of aggressive behavior of male rats.

Aggression↗
PubMed1994

Effects of chronically high doses of the anabolic androgenic steroid, testosterone, on intermale aggression and sexual behavior in male rats.

To determine if chronic exposure to high doses of anabolic androgenic steroids (AAS) increase aggression and sexual activity in gonadally intact rats, we administered SC injections of testosterone propionate (TP: 1 mg) or propylene glycol (PG: as a vehicle control) three times per week for 10 consecutive weeks. Weekly tests for male copulation were conducted by pairing each male with a sexually receptive female in a glass arena and recording various parameters of copulation. Chronic treatment with TP did not alter any parameter of male copulation including ejaculation and post ejaculatory interval. Sexually experienced males were tested once per week for intermale aggression in a neutral environment. For aggression tests, each experimental animal was placed into an arena with an opponent male for 15 min. The opponent, a gonadally intact male, was used only for the purpose of the aggression test. Frequencies of dominance, submissive, threat, and fight postures, as well as approaches were scored for each animal. TP-treated males did not differ in body weight from PG-treated males, suggesting that the increased aggression was not due to increased body mass. The results of this study show that chronic exposure to the anabolic androgenic steroid, testosterone, potentiates male aggressive response patterns but does not alter male sexual behavior or body weight.

Aggression↗
PubMed1996

Testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.

In many species, testosterone treatment facilitates offensive aggression tested in resident-intruder models. As the mechanisms of action of testosterone remain unclear, we hypothesized that testosterone interacts with neurotransmitter systems involved in the regulation of offensive aggression. We tested this hypothesis with the vasopressinergic system in golden hamsters in three separate experiments. First, we compared the density of V1 vasopressin (VAP) receptor binding between castrated animals treated with testosterone and their untreated controls. The most noticeable difference was found within the ventrolateral hypothalamus (VLH), a site involved in the control of aggression in several species of mammals. Within this area, V1 AVP receptor binding disappeared after castration, while being maintained by testosterone-treatment. Second, we tested behavioral effects of AVP within the VLH. Microinjections of AVP (100 nl, 1 or 100 microM) within the VLH accelerated the onset of offensive aggression in testosterone-treated animals. However, AVP-injected animals did not bite more than their vehicle-injected controls. Third, microinjections of AVP failed to activate offensive aggression in animals deprived of testosterone. As AVP receptors appeared to overlay previously described distributions of androgen and estrogen receptors in golden hamsters, we propose that testosterone facilitates the onset of offensive aggression, at least partly, through an activation of AVP receptors within the VLH.

Aggression↗
PubMed1982

Alterations in trace amine and trace acid concentrations in isolated aggressive mice.

We have used an animal model of aggression, the isolation syndrome in mice, to examine the possible role of the trace amines, beta-phenylethylamine (PEA), meta-tyramine (m-TA) and para-tyramine (p-TA) in aggressive behaviour. The brain, plasma and urinary levels of PEA, m-TA and p-TA, and their respective major acid metabolites, phenylacetic acid (PAA), meta-hydroxyphenylacetic acid (m-HPA) and para-hydroxyphenylacetic acid (p-HPA) were measured in isolated aggressive mice (after fighting), and in group housed controls. The urinary levels of PEA, m-TA, PAA, m-HPA and p-HPA, and the plasma levels of PAA and p-HPA were significantly lower in isolated aggressive mice. Similarly, the whole brain levels of PEA, p-TA, PAA and p-HPA tended to be reduced. In contrast, the brain levels of m-TA and m-HPA tended to increase. It should be noted, however, that the present procedure did not dissociate the stress and aggression components of the isolation syndrome, and, therefore, further experiments are required to determine whether the observed neurochemical changes are functionally related to increased aggression.

Aggression↗
PubMed1984

Irritable aggression induced by delta 9-tetrahydrocannabinol in rats pretreated with 6-hydroxydopamine.

Administration of delta 9-tetrahydrocannabinol (THC) to grouped rats injected intraventricularly with 6-hydroxydopamine (6-OHDA) produced violent fighting accompanied by remarkable hyperirritability. This behavior was induced reproducibly from the 10th to 100th postoperative days. It was shown that this irritable aggression could be measured continuously and quantitatively in terms of degree of activity and/or vocalization using a newly designed analyzer. The effect of THC differed markedly from the action of apomorphine and methamphetamine in 6-OHDA pretreated rats. Apomorphine induced irritable aggression but not vigorous vocalization. On the other hand, methamphetamine induced much less irritable aggression than apomorphine-induced aggression. It is assumed that a THC-invoked imbalance in catecholamine agonistic and serotonin antagonistic action brought about by activation of supersensitized catecholaminergic receptor was operating to produce the aggression. Specifically, hypoactivity of serotonergic neurons might play a key role in the occurrence of THC-induced irritable aggression.

Aggression↗
PubMed1985

Benzodiazepine-receptor mediated inhibition of isolation-induced aggression in mice.

The effects of a benzodiazepine receptor agonist (diazepam), antagonist (Ro 15-1788), and an "active" antagonist [inverse agonist] (3-carboethoxy-beta-carboline) were examined in an isolation-induced model of aggression. Diazepam (4 mg/kg) and 3-carboethoxy-beta-carboline (10 mg/kg), but not Ro 15-1788, significantly inhibited aggressive behavior in this model. Ro 15-1788 (10 mg/kg) reduced the anti-aggressive actions of both diazepam and 3-carboethoxy-beta-carboline, while mice treated with a combination of diazepam and 3-carboethoxy-beta-carboline had aggression scores increased to values not significantly different from vehicle treated mice. These findings suggest that both diazepam and 3-carboethoxy-beta-carboline have anti-aggressive properties in the isolation-induced model of aggression which are mediated through CNS benzodiazepine receptors.

Aggression↗
PubMed1987

Involvement of brain transmitters in the modulation of shock-induced aggression in rats by propranolol and related drugs.

(+/-)Propranolol (1, 3, 10 and 30 mg/kg) exhibited a differential effect on footshock aggression (FSA) in rats. Lower doses (1 and 3 mg/kg) of the drug facilitated FSA, whereas an inhibitory effect was observed with higher doses (10 and 30 mg/kg) of the same. (+)Propranolol (30 mg/kg) and UM-272 (1 and 10 mg/kg) as well as physostigmine (0.1 and 0.5 mg/kg) all produced inhibition of FSA. Similar FSA inhibitory effects were also observed with salbutamol (1 and 5 mg/kg). Pretreatment with atropine and not methylatropine attenuated the anti-aggressive effect of (+/-)propranolol (10 mg/kg) without appreciably altering the facilitatory effect (1 mg/kg) of the drug on FSA. In addition, at the anti-aggressive doses, (+/-)propranolol (10 mg/kg) and UM-272 (10 mg/kg), significantly inhibited brain cholinesterase enzyme activity when compared to saline controls. (+/-)Propranolol (10 mg/kg) also inhibited significantly the aggression induced by reserpine-apomorphine treatment. It is inferred that a central cholinergic and dopaminergic mechanism is involved in the anti-aggressive effect of (+/-)propranolol, whereas the low dose induced facilitation of affective aggression could be attributed to central beta-adrenoceptor blockade.

Acetylcholinesterase↗
PubMed1987

The effect of raising or lowering tryptophan levels on aggression in vervet monkeys.

Social groups of vervet monkeys (Cercopithecus aethiops) were given amino acid mixtures that were tryptophan-free (T-), nutritionally balanced (B), or contained excess tryptophan (T+). The T- mixture caused a marked decrease in plasma tryptophan and the T+ mixture a large increase. Behavioral observations were made on the animals after administration of the amino acid mixtures both during spontaneous activity and while the (fasted) animals were competing for food newly placed in the feeder. The only effect of the biochemical manipulations on spontaneous aggression was an increase in aggression of the male animals with the T- mixture. During competition for the food the T- mixture increased and the T+ mixture decreased aggression in the males, while the T+ mixture decreased aggression in females. These data indicate that brain 5-hydroxytryptamine can influence aggression in a primate and suggest that altered tryptophan levels can influence aggression more reliably at higher levels of arousal.

Aggression↗
PubMed1990

Sexual differentiation and the effects of alcohol on aggressive behavior in mice.

Male and female mice are differentially sensitive to the effects of alcohol on aggressive behavior. We investigated the role of testosterone during sexual differentiation in determining sex differences in alcohol effects on aggression. On the day of birth male mice were castrated or sham-operated. Neonatal female mice were injected with 250 micrograms of testosterone propionate (TP) or the oil vehicle. At approximately 75 days of age the mice which had not been gonadectomized at birth were gonadectomized. Control males and androgenized female mice then received 7.5 mm Silastic capsules containing testosterone, SC. Aggressive behavior toward an intruder was assessed following administration of ethanol (0.1-3.0 g/kg) or water, PO. Neonatally sham-gonadectomized male mice had a significant increase in aggressive behavior following administration of 1.0 g/kg alcohol, with no significant suppression of aggression at 3.0 g/kg. Neonatally androgenized female mice showed neither the male-typical response to adult testosterone and alcohol, nor did they show the female-typical response. Neonatally gonadectomized males showed an alcohol dose response curve that was similar to that of androgenized females. Postnatal testosterone did not appear to completely determine the male- and female-typical responses to alcohol on aggression. The critical period for this sexually dimorphic response to alcohol and testosterone may be primarily prenatal.

Aggression↗
PubMed1991

Effects of serotonergic agents on isolation-induced aggression.

A series of serotonergic agents were assessed for their ability to antagonize isolation-induced aggression and their activity to disrupt performance in the rotorod motor coordination test. All compounds with 5-HT1A activity [buspirone, gepirone, ipsapirone, tandospirone (SM-3997), 8-OH-DPAT, Wy-48,723, BMY-7378, Wy-47,846] reduced aggression at doses below those which produced debilitation in the rotorod motor coordination test. In addition, the 5-HT3 antagonist zacopride failed to attenuate aggression or produce debilitation at any of the doses tested; however, the 5-HT2 antagonist ritanserin inhibited aggressive behavior at a high dose which was not debilitating. Benzodiazepines (chlordiazepoxide, diazepam and lorazepam), and antidepressant (desipramine) and an antipsychotic (haloperidol) reduced aggressive behavior only at debilitating doses. Activity at the 5-HT1A receptor, and possibly nonsedative anxiolytic activity, appears to be related to antagonism of isolation-induced aggression.

Aggression↗
PubMed1995

Noradrenergic denervation attenuates desipramine enhancement of aggressive behavior in isolated mice.

The effects of denervation of central noradrenergic system on the desipramine-induced enhancement of aggressive behavior were examined in long-term isolated mice. Consistent with previous reports, desipramine (10 mg/kg, IP) significantly increased the duration of aggressive behavior in isolated mice. Pretreatment of isolated mice with DSP-4, a selective noradrenaline neurotoxin, significantly attenuated the enhancing effect of desipramine on aggressive behavior without affecting the basal aggressive responses. This effect appeared concomitant with decrease of noradrenaline levels in the cortex, hippocampus, cerebellum and hypothalamus (78%, 75%, 57%, and 17%, respectively). DSP-4 did not significantly affect dopamine or 5-HT levels in these regions. These results suggest that noradrenergic terminals originating mainly from the locus coeruleus play an important role in the desipramine enhancement of aggressive behavior, but not in the basal aggressive behavior of isolated mice.

Aggression↗
PubMed1994

Time-dependent effects of PCPA on social aggression in chicks.

We investigated the effects of para-chlorophenylalanine (PCPA), a serotonin (5-HT) antagonist, on social aggression and brain neurochemistry in young domestic chickens (Gallus domesticus). In Experiment 1, the effects of four different doses of PCPA (0, 100, 200, and 400 mg/kg) were examined for 3 days after injection. Immediately after PCPA injection, aggressive pecking was low and then increased over the 3-day test period. PCPA significantly decreased 5-HT, 5-hydroxyindoleacetic acid (5-HIAA), and 5-HT turnover. In addition, the frequency of aggression was negatively correlated with levels of 5-HIAA. In Experiment 2, the time-dependent effects of a single 400-mg/kg dose of PCPA were examined for 5 and 7 days after drug exposure. PCPA-treated chicks observed for 5 days after injection had significantly greater frequencies of aggression 4 days following drug exposure and significantly reduced 5-HT levels when measured on the next day. Similarly, chicks observed for 7 days exhibited significantly elevated aggression 5 days after injection, after which their pecking decreased to control levels on days 6 and 7. Coinciding with this behavioral pattern, 5-HT levels from these PCPA-treated chicks when assessed 7 days after drug exposure were the same as those for control birds. We concluded that PCPA increased social aggression in birds, an effect that diminished as brain 5-HT levels recovered over a 1-week period.

Aggression↗
PubMed1991

Serotonin receptor sensitivity and aggression.

This study investigated the relationship between increased serotonin (5-hydroxytryptamine, 5HT) receptor sensitivity and human aggression. A low oral dose of meta-chlorophenylpiperazine (MCPP), a postsynaptic 5HT receptor agonist, was administered in a placebo-controlled design to depressed (n = 22) and panic disorder (n = 20) patients classified with or without signs of outwardly directed aggression, patients with a history of suicide attempts (inwardly directed aggression) (n = 11), and normal controls (n = 19). Hormones under 5HT control were measured at 30-min intervals. Results were as follows: (1) MCPP did not induce or reduce anger, (2) patients with outwardly directed aggression did not have significantly greater MCPP-induced cortisol or prolactin release than did patients without signs of outwardly directed aggression, (3) patients with a history of suicide attempts did not have significantly greater MCPP-induced cortisol or prolactin release than did normal controls, and (4) MCPP-induced hormone release was unrelated to measures of aggression.

Adult↗