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PubMed1999

Natural history of aggressive behaviour in dementia.

OBJECTIVE: This article analyses changes in aggressive behaviour throughout the course of dementia. DESIGN: Prospective, 10 year, longitudinal study of aggressive behaviour in dementia, with autopsy follow-up. SETTING: Subjects with dementia, living at home with a carer, Oxfordshire, UK. PARTICIPANTS: Ninety-nine people with dementia (Alzheimer's disease and/or vascular dementia) who were living at home with a carer. MEASURES: At 4-monthly intervals, the carers were interviewed about the subjects and the subjects were assessed cognitively. Subjects' behaviour was assessed using the Present Behavioural Examination. This is an investigator-based, semi-structured interview consisting of eight main sections monitoring behavioural and psychological change. Eight different aspects of aggressive behaviour were assessed in detail and comparison made with other relevant factors. RESULTS: Verbal aggression is the most common and longest lasting form of aggressive behaviour. Aggressive resistance and physical aggression are most likely to persist until death. Intimate care is the main factor precipitating aggressive behaviour. There are no correlations between any type of aggressive behaviour and age, gender or time since onset of dementia. CONCLUSIONS: Aggressive behaviour creates problems for carers. In general, the physical types of aggressive behaviour are most prevalent in people with more severe dementia.

Aged↗
PubMed1999

Ovarian hormones influence territorial aggression in free-living female mountain spiny lizards.

Females are aggressive in many species but relatively little is known about the hormonal basis of female aggression, especially in free-living animals. Female mountain spiny lizards aggressively defend territories from other females. Previously, we showed that plasma levels of testosterone (T) and estradiol (E) are positively associated with levels of female aggression. Here, we manipulated hormone levels in free-living females and examined aggression expressed by females returned to their natural territories. Females received one of the following: (1) ovariectomy + empty implant (OVEX), (2) ovariectomy + T implant (T-IMP), or (3) sham surgery + empty implant (SHAM). OVEX females had reduced plasma levels of E but not T relative to SHAM females. T-IMP females had elevated plasma levels of T. Levels of display and aggression in OVEX females were reduced relative to SHAM females. T-IMP females had restored levels of display behavior although, unlike SHAM, no T-IMP females expressed the overt aggressive behavior of charging. These data are most consistent with the hypothesis that an ovarian factor such as E promotes female aggression, since ovariectomy reduced both plasma E and aggression but had no effect on plasma T. The results from the T-IMP females are also consistent with this hypothesis if we assume that the effects of T are due to aromatization to E in target tissues. The data do not rule out a role for T in promoting female aggression since T-implants resulted in elevated plasma T and restored display behaviors. This study represents one of the first studies examining the hormonal basis of female aggression in free-living females.

Aggression↗
PubMed2000

Short-day increases in aggression are inversely related to circulating testosterone concentrations in male Siberian hamsters (Phodopus sungorus).

Many nontropical rodent species display seasonal changes in both physiology and behavior that occur primarily in response to changes in photoperiod. Short-day reductions in reproduction are due, in part, to reductions in gonadal steroid hormones. In addition, gonadal steroids, primarily testosterone (T), have been implicated in aggression in many mammalian species. Some species, however, display increased aggression in short days despite basal circulating concentrations of T. The goal of the present studies was to test the effects of photoperiod on aggression in male Siberian hamsters (Phodopus sungorus) and to determine the role of T in mediating photoperiodic changes in aggression. In Experiment 1, hamsters were housed in long and short days for either 10 or 20 weeks and aggression was determined using a resident-intruder model. Hamsters housed in short days for 10 weeks underwent gonadal regression and displayed increased aggression compared to long-day-housed animals. Prolonged maintenance in short days (i.e., 20 weeks), however, led to gonadal recrudescence and reduced aggression. In Experiment 2, hamsters were housed in long and short days for 10 weeks. Half of the short-day-housed animals were implanted with capsules containing T whereas the remaining animals received empty capsules. In addition, half of the long-day-housed animals were castrated whereas the remaining animals received sham surgeries. Short-day control hamsters displayed increased aggression compared to either castrated or intact long-day-housed animals. Short-day-housed T treated hamsters, however, did not differ in aggression from long-day-housed animals. Collectively, these results confirm previous findings of increased aggression in short-day-housed hamsters and suggest that short-day-induced increases in aggression are inversely related to gonadal steroid hormones.

Aggression↗
PubMed2001

20-hydroxyecdysone causes increased aggressiveness in female American lobsters, Homarus americanus.

Lobsters become transiently more aggressive before ecdysis. This aggressiveness accompanies an increase in hemolymph titers of 20-hydroxyecdysone (20-HE). Combats between intermolt female lobsters, injected with premolt levels of 20-HE, and larger, saline-injected opponents were videotaped. Aggressive, defensive, and avoidance behaviors were ranked according to aggressiveness in a Rank of Aggression hierarchy, which included opponent-directed and (nonopponent) redirected behaviors. Treated animals performed more and more highly aggressive behaviors than saline-injected controls. Opponents of treated animals performed fewer aggressive behaviors than saline-injected control opponents. Controls performed more defensive behaviors than treated animals, when redirected behaviors were considered. Differences in avoidance behaviors among the four types of combatants were not significant. The total aggressive content was the same in treated and control fights, but the interactions between combatants in the two fights were significantly different. Treated animals were equally as aggressive and defensive as their opponents; controls were relatively less aggressive and more defensive than their opponents. These results correlate with molt-cycle variations in behavior, 20-HE titers, and the effects of 20-HE and molt-differentiated hemolymph on the claw opener muscle. They suggest that 20-HE orchestrates intrinsic, cellular, and nuclear events that produce the molt-cycle transformations in agonistic behavior and aggressive state of lobsters.

Aggression↗
PubMed1989

Reactive and proactive aggression in childhood: relations to peer status and social context dimensions.

Although there has been an accumulation of evidence to suggest a link between peer-directed aggression and social rejection, little attention has been given to the relations between specific subtypes of aggressive behavior and social rejection. The purpose of this investigation was to examine the relations between two subtypes of aggressive behavior (reactive and proactive aggression) and children's classroom peer status. The reciprocity of each of these subtypes of aggressive behavior and the social contexts in which these behaviors occur were also examined. Assessments of each of these forms of aggression among 70 boys (ages 5 and 6) were conducted using direct observations and teacher ratings. In general, directing reactive aggressive behavior toward peers was associated with social rejection, while utilization of instrumental aggression was positively related to peer status. The findings also indicated that directing proactive forms of aggression toward peers was related to being the target of proactive aggression. Finally, among older boys, both subtypes of aggression were more likely to occur during rough play than during any other type of play activity.

Aggression↗
PubMed1999

Aggression heightened by alcohol or social instigation in mice: reduction by the 5-HT(1B) receptor agonist CP-94,253.

RATIONALE: Models of heightened aggression may be particularly relevant in exploring pharmacological options for the clinical treatment of aggressive and impulsive disorders. OBJECTIVES: To investigate and compare the effects of a 5-HT(1B) selective agonist, CP-94,253, on aggression that was heightened as a result of 1) social instigation or 2) alcohol treatment. METHODS: Male CFW mice were administered 1.0 g/kg EtOH and were subsequently confronted by an intruder in their home cage. In a separate experimental procedure, resident male mice were instigated to aggressive behavior by brief exposure to a provocative stimulus male. To test the hypothesis that activation of the 5-HT(1B )receptor subtype would preferentially attenuate heightened aggression, in comparison to the moderate levels of species-typical aggressive behaviors, the selective agonist, CP-94,253 (1.0-30 mg/kg, IP), and antagonists to the 5-HT(1B) (GR 127935; 10 mg/kg, IP) and the 5-HT(1A) receptor (WAY 100,635; 0.1 mg/kg IP) were used. RESULTS: CP-94,253 suppressed non-heightened aggressive behavior (ED(50)=7.2 mg/kg ). GR 127935, but not WAY 100,635 shifted the ED(50) for CP-94,253 to 14.5 mg/kg. Importantly, the anti-aggressive effects of CP-94,253 were not accompanied by locomotor sedation. Alcohol-heightened and instigation-heightened aggression were suppressed at lower doses than those necessary to suppress non-heightened aggression (ED(50)=3. 8 and 2.7 mg/kg, respectively). CONCLUSIONS: The current results support the hypothesis that activation of 5-HT(1B) receptors modulates very high levels of aggressive behavior in a pharmacologically and behaviorally specific manner.

Aggression↗
PubMed2002

Acute effects of baclofen, a gamma-aminobutyric acid-B agonist, on laboratory measures of aggressive and escape responses of adult male parolees with and without a history of conduct disorder.

RATIONALE: The possible role of gamma-aminobutyric acid (GABA) in human aggression was evaluated by administering baclofen, a GABA-B agonist and comparing the effects on laboratory measures of aggression and escape among subjects with and without a history of conduct disorder. METHODS: Twenty male subjects with a history of criminal behavior participated in experimental sessions, which measured aggressive and escape responses. Ten subjects had a history of childhood conduct disorder (CD+) and ten control subjects had no history of CD. Aggression was measured using the point subtraction aggression paradigm (PSAP), which provides subjects with aggressive, escape, and monetary-reinforced response options. RESULTS: Acute doses (0.07, 0.14 and 0.28 mg/kg) of baclofen had remarkably different effects on aggressive responses among CD+ subjects relative to control subjects. Aggressive responses of CD+ subjects decreased, while aggressive responses of control subjects increased following baclofen administration. Baclofen decreased escape responses for both CD+ and control subjects. No changes in monetary-reinforced responses were observed, indicative of no central nervous system stimulation or sedation. CONCLUSIONS: The GABA-B agonist baclofen suppressed aggressive responses in subjects with a history of childhood CD, while producing the opposite effect in control subjects. These suggest a possible unique role for GABA in the regulation of aggression in CD+ population.

Adult↗
PubMed2002

Aggressive behavior as a reinforcer in mice: activation by allopregnanolone.

RATIONALE: The neurobiological mechanisms that underlie the motivation to engage in an aggressive confrontation remain to be investigated. OBJECTIVE: The objective was to develop a method to differentiate pharmacologically the performance elements of aggressive behavior from behaviors that precede an aggressive encounter. METHODS AND RESULTS: Male CFW mice were housed as "residents" and trained to poke their nose in a hole in a panel placed into the home cage. After fulfilling a specific response requirement, an "intruder" male mouse was introduced for a brief aggressive encounter. In experiment I, the mice were maintained on a fixed ratio schedule of ten responses (FR10) and after stable responding, extinction and stimulus control were assessed by switching the active hole in an ABA design. In experiment II and III, the mice were maintained on a fixed interval schedule of 10 min (FI10 min) and responded with accelerating rates towards the end of the interval (mean index of curvature was 0.37). In experiment III, the mice were given the GABA(A) receptor positive modulator allopregnanolone (5.6-17 mg/kg or vehicle, IP), before responding on an FI10 min schedule reinforced by a 5-min aggressive encounter. Allopregnanolone had bitonic effects on FI responding and aggressive behavior. The low dose of allopregnanolone nearly doubled overall response rate without affecting the index of curvature, attack bites or sideways threats. The moderate dose increased attack behaviors by about 45% and had little effect on response rate and the index of curvature. In contrast, the higher dose decreased the index of curvature but had no effect on aggressive behavior or overall response rate. CONCLUSIONS: These data support previous demonstrations that certain GABA(A) positive modulators heighten aggressive behavior. Moreover, examining operant responding that is reinforced by the opportunity for aggression, it may be possible to dissociate pharmacological effects on the behaviors leading up to an aggressive encounter from their effects on specific aggressive acts.

Aggression↗
PubMed2003

Angry cognitive bias, trait aggression and impulsivity in substance users.

RATIONALE: According to cognitive theory, people who are aggressive expect angry responses to ambiguous situations. Increased aggression has been reported a few days or weeks following use of MDMA (ecstasy). This may relate to low 5-HT release, and so a 5-HT challenge may increase cognitive bias towards anger differentially in MDMA users and non-users. OBJECTIVES: To investigate whether: (1) measures of anger and aggression will correlate with processing time of angry material and with generation of aggressive responses and (2) tryptophan challenge in people abstinent from MDMA and controls will affect angry cognitive bias. METHODS: Thirty-two current MDMA users abstinent for 3 weeks, 32 ex-users abstinent for longer than 1 year and 32 non-MDMA substance users were recruited. Trait measures were administered before and state measures before and 5 h after an amino acid drink, depleted or augmented with tryptophan. After the drink, subjects undertook a computer task, which involved reading ambiguous short stories. Reading times to a key sentence describing an angry or non-angry reaction were recorded and subjects wrote a continuing sentence for half the stories. RESULTS: Subjects were faster to process angry than non-angry reactions, indicating the presence of angry cognitive bias. Trait anger and aggression were correlated with processing time of angry relative to non-angry reactions, particularly in the current users. Impulsivity was correlated with non-specific speed of response. Subjects wrote more aggressive sentences after an angry reaction. Tryptophan depletion tended to increase aggressive content. Trait aggression was correlated with aggressive content following non-angry reactions. CONCLUSIONS: Evidence of angry cognitive bias was shown in this group of substance users, which was not specific to MDMA use. People high on trait aggression were more likely to expect an angry reaction to an ambiguous situation and to generate more written aggression when this did not occur.

Aggression↗
PubMed2003

Reduced isolation-induced aggressiveness in mice following NAALADase inhibition.

RATIONALE: Long-term individual housing increases aggressive behavior in mice, a condition termed isolation-induced aggression; this aggressiveness is reduced by some antidepressants and anxiolytics. NMDA antagonists also inhibit isolation-induced aggression in mice. The enzyme N-acetylated-alpha-linked acidic dipeptidase (NAALADase) hydrolyzes the neurotransmitter N-acetylaspartylglutamate (NAAG) to form glutamate and N-acetylaspartate; NAAG acts as a partial NMDA agonist as well as a full agonist at the presynaptic metabotropic glutamate receptor 3 (mGluR3), where it acts to reduce glutamate release. OBJECTIVE: We postulated that NAALADase inhibition would reduce isolation-induced aggression in mice. METHODS: We tested whether acute exposure to the NAALADase inhibitor 2-[[hydroxy[2,3,4,5,6-pentafluorophenyl)methyl]phosphinyl]methyl] pentanedioic acid (GPI-5232), administered 30 min prior to a social interaction test, would inhibit aggressive behavior in SJL mice that had been individually housed long term. RESULTS: Administration of GPI-5232 (30 mg/kg, IP) inhibited initiation of aggressive behavior, indicated by greater latencies to display tail-rattling, attack and biting, and by fewer mice initiating aggressive behavior, compared to mice that received vehicle. In addition, GPI-5232 treated mice had fewer tail-rattling responses to a non-aggressive conspecific. CONCLUSIONS: The effectiveness of GPI-5232 in this animal model suggests that NAALADase inhibition may be a novel therapeutic approach to reduce or inhibit heightened aggressiveness, and possibly to treat aggressive behavior associated with psychiatric disorders.

Aggression↗
PubMed2000

Effects of the NMDA receptor channel blockers memantine and MRZ 2/579 on morphine withdrawal-facilitated aggression in mice.

RATIONALE: Opioid withdrawal is known to facilitate aggressive behavior in laboratory rodents. Aggression develops as the somatic signs disappear and thus may reflect protracted withdrawal-related behavioral alterations. Antagonists acting at the NMDA receptor are known to attenuate the expression of morphine withdrawal syndrome in laboratory animals. OBJECTIVE: The present study aimed to evaluate the effects of low-affinity NMDA receptor channel blockers (memantine and MRZ 2/579) on aggression facilitated by morphine withdrawal in mice. METHODS: Significant increases in aggressive behavior were observed 48 h after repeated morphine administration (8 days, b.i.d., 10-80 mg/kg, s.c.) was discontinued. Separate groups of mice were treated intraperitoneally with vehicles or different doses of memantine (1, 3, 10 or 30 mg/kg) or MRZ 2/579 (1, 3 or 10 mg/kg) 48 h after the last morphine injection. RESULTS: Both compounds dose-dependently reduced the expression of aggressive behavior while having no significant effect upon the intensity of non-aggressive social contacts. Memantine significantly diminished the occurrence of all recorded components of aggressive behavior (attacks/bites, threats, tail rattling) while MRZ 2/579 affected mainly the appetitive events of aggressive bursts (threats, tail rattling). For both compounds, anti-aggressive effects occurred at dose levels that did not produce motor impairment in the Rotarod test. CONCLUSIONS: Taken together with the evidence on the lack of selective anti-aggressive effects of these drugs in morphine-naive mice, attenuation of the aggression observed in the present study may be due to specific interaction with morphine withdrawal-triggered processes.

Aggression↗
PubMed2001

Oral drug self-administration in the home cage of mice: alcohol-heightened aggression and inhibition by the 5-HT1B agonist anpirtoline.

RATIONALE: In order to model heightened aggression after alcohol consumption and to study the inhibitory influence of 5-HT1B receptors on drinking and fighting, an experimental procedure should enable self-administration of precise amounts of alcohol in a limited period of time before an aggressive confrontation. OBJECTIVES: To design a new device that can reinforce operant responding by the delivery of sweet alcohol in the resident mouse home cage, where aggressive behavior toward an intruder can subsequently be examined, and to demonstrate inhibition of alcohol-heightened aggression by 5-HT1B receptor agonist treatment. METHODS: Within one experimental session, all singly housed CFW male mice (n=26) performed a nose-poke response that was reinforced by 0.05 ml sucrose. Using the sucrose fading technique, eventually the mice consumed a 6% ethanol/4% sucrose solution after each fifth nose poke during daily 15-min experimental sessions. The number of ethanol reinforcements was adjusted so that 0.6, 1.0, 1.7, and 3.0-g/kg doses were consumed in 15 min or less. Assays confirmed blood alcohol levels at 68.1 mg/dl for intake of 1.0 g/kg. After consuming a specific dose of ethanol in the form of a fixed number of response-dependent deliveries, the response panel was removed from the home cage and, 15 min later, the resident confronted a male intruder. Anpirtoline was administered either before alcohol self-administration or before the aggressive confrontation. RESULTS: After being reinforced with 1.0 g/kg or 1.7 g/kg sweet ethanol, the mice significantly increased attack and threat behavior relative to their aggressive behavior following sucrose or water consumption only. Treatment with the 5-HT1B receptor agonist anpirtoline (0.125, 0.25, 0.5 mg/kg, i.p.) before the confrontation decreased alcohol-heightened aggression and species-typical aggression in the absence of changes in other elements of the behavioral repertoire. Anpirtoline affected ethanol-reinforced behavior only at doses that were 5-10 times higher than those producing anti-aggressive effects. CONCLUSIONS: Self-administration of alcohol in the home cage of mice is readily accomplished with the aid of a simple, removable panel. The effective inhibition of high levels of aggressive behavior due to alcohol consumption after anpirtoline treatment confirm the 5-HT1B receptor as a critical site in the termination of aggression.

Aggression↗
PubMed1988

Activation of aggression in female rats by normal males and by castrated males with testosterone implants.

Female hooded rats were continuously housed with an intact male, a castrated male with subcutaneous testosterone implants, or two other females. At weekly intervals over a 10-week period, the cagemate(s) and pups were removed and aggression by the female toward an unfamiliar female intruder was observed over a 15-min period. On the 11th week each female was subjected to this intruder test in an unfamiliar cage. On the 12th week, a final test was conducted in each female's living cage with a male rather than a female as the intruder. The aggressive behaviors recorded were attacks, bites, on-top, and piloerection. Females housed with normal males displayed a significant increase in aggression prior to parturition. Their aggressiveness persisted through the 10th test with peaks at parturition and the start of lactation. Females housed with castrated males also displayed significant increases in aggression but without the peaks associated with parturition and lactation. Their aggressiveness also persisted throughout the test period. Females housed with other females showed a small increase in aggression over weeks. All groups showed virtually no aggression in the unfamiliar cage. All females displayed some aggression toward a male intruder but the level of aggression was highest in maternal females. The results demonstrate that aggression qualitatively similar to that displayed following parturition and during lactation can be elicited in nulliparous females.

Aggression↗
PubMed2004

Elevated stress sensitivity in corticotropin-releasing factor receptor 2 deficient mice decreases maternal, but not intermale aggression.

Maternal aggression is a form of aggression towards intruders by lactating females that is critical for defense of offspring. During lactation, fear and anxiety are reduced, the CNS is less responsive to the anxiogenic neuropeptide, corticotropin-releasing factor (CRF), and central injections of CRF inhibit maternal aggression. Together, these previous findings suggest that decreased CRF neurotransmission during lactation supports normal maternal aggression expression. Recent work indicates that mice deficient in CRF receptor 2 (CRFR2) display increased anxiety-like behaviors, have a hypersensitive stress response, and overproduce CRF. In this study, we examined both maternal and intermale aggression in wild-type (WT) and CRFR2-deficient mice. CRFR2-mutant mice exhibited significant deficits in maternal aggression on postpartum Day 4 relative to WT mice in terms of percentage displaying aggression, mean number of attacks, and mean time in aggressive encounters. However, time sniffing male intruder, pup retrieval, number of pups, and performance on the elevated plus maze were similar between genotypes. In contrast, intermale aggression did not differ between genotype in any measure on any of three consecutive test days. For neither form of aggression did sites of attacks on the intruder differ between genotype. Taken together, the results suggest that differences in stress sensitivity and the overproduction of CRF of the knockout (KO) mice specifically affects maternal, but not intermale aggression.

Aggression↗
PubMed2006

Lasting changes in neuronal activation patterns in select forebrain regions of aggressive, adolescent anabolic/androgenic steroid-treated hamsters.

Repeated exposure to anabolic/androgenic steroids (AAS) during adolescence stimulates high levels of offensive aggression in Syrian hamsters. The current study investigated whether adolescent AAS exposure activated neurons in areas of hamster forebrain implicated in aggressive behavior by examining the expression of FOS, i.e., the protein product of the immediate early gene c-fos shown to be a reliably sensitive marker of neuronal activation. Adolescent AAS-treated hamsters and sesame oil-treated littermates were scored for offensive aggression and then sacrificed 1 day later and examined for the number of FOS immunoreactive (FOS-ir) cells in regions of the hamster forebrain important for aggression control. When compared with non-aggressive, oil-treated controls, aggressive AAS-treated hamsters showed persistent increases in the number of FOS-ir cells in select aggression regions, namely the anterior hypothalamus and lateral septum. However, no differences in FOS-ir cells were found in other areas implicated in aggression such as the ventrolateral hypothalamus, bed nucleus of the stria terminals, central and/or medial amygdala or in non-aggression areas, such as the samatosensory cortex and the suprachiasmatic nucleus. These results suggest that adolescent AAS exposure may constitutively activate neurons in select forebrain areas critical for the regulation of aggression in hamsters. A model for how persistent activation of neurons in one of these brain regions (i.e., the anterior hypothalamus) may facilitate the development of the aggressive phenotype in adolescent-AAS exposed animals is presented.

Aggression↗
PubMedDate not supplied

Predictors of aggression on the psychiatric inpatient service.

Patients with severe mental illness are at increased risk to commit acts of aggression in the inpatient hospital setting. Aggressive behaviors have severe negative consequences for the patient, victims, clinical staff, and the therapeutic community as a whole. While risk factors of community and inpatient aggression overlap, many predictive factors diverge between the two settings. For example, while medication noncompliance has been a robust predictor of community aggression, this factor has little predictive value for inpatient settings where patients' pharmacotherapy is closely monitored. Relatively fewer investigators have examined a wide range of predictive factors associated with aggressive acts committed on the psychiatry inpatient service, often with conflicting results. The present study examined demographic, clinical, and neurocognitive performance predictors of self, other, object, and verbal aggressiveness in 118 acute inpatients. Results revealed that the arrival status at the hospital (voluntary vs involuntary), female gender, and substance abuse diagnosis were predictors of verbal aggression and aggression against others. Impaired memory functioning also predicted object aggression. Fewer symptoms, combined with higher cognition functioning, however, were significant predictors of self-aggressive acts committed on the inpatient service. The need for relating predictors of specific types of aggressiveness in schizophrenia is discussed.

Adult↗
PubMed2004

c-fos Changes following an aggressive encounter in female California mice: a synthesis of behavior, hormone changes and neural activity.

Although there has been growing interest in the neuroanatomical and physiological mechanisms underlying aggressive behavior, little work has focused on possible mechanisms controlling natural plasticity in aggression. In the current study, we used naturally occurring changes in aggression level displayed by female Peromyscus californicus across the estrous cycle and parallel changes in c-fos expression to examine possible brain regions involved in mediating this plasticity. We found that c-fos expression was increased in females exposed to a conspecific female intruder compared with control females in numerous brain regions thought to be involved in the control of aggression. More importantly, we found that c-fos increased in the bed nucleus of the stria terminalis (BNST) and ventral lateral septum (LSv) only in the more aggressive, diestrous females, and not in the less aggressive, proestrous and estrous females. Conversely, c-fos increased in the medial amygdala (MeA) across all stages of estrus compared with controls, suggesting the MeA is not involved in mediating changes in individual levels of aggression. Moreover, we found correlations between several measures of aggression and c-fos expression in the BNST and LSv but not the MeA, again suggesting a role in mediating aggression plasticity for the former two but not the latter brain region. We further hypothesize that the BNST and the LSv may be involved more generally in mediating natural changes in aggression, such as increases often observed after individuals win aggressive interactions against conspecifics.

Aggression↗
PubMed2004

Territorial aggression, circulating levels of testosterone, and brain aromatase activity in free-living pied flycatchers.

Testosterone (T) is a critical endocrine factor for the activation of many aspects of reproductive behavior in vertebrates. Castration completely eliminates the display of aggressive and sexual behaviors that are restored to intact level by a treatment with exogenous T. There is usually a tight correlation between the temporal changes in plasma T and the frequency of reproductive behaviors during the annual cycle. In contrast, individual levels of behavioral activity are often not related to plasma T concentration at the peak of the reproductive season suggesting that T is available in quantities larger than necessary to activate behavior and that other factors limit the expression of behavior. There is some indication from work in rodents that individual levels of brain aromatase activity (AA) may be a key factor that limits the expression of aggressive behavior, and in agreement with this idea, many studies indicate that estrogens produced in the brain by the aromatization of T may contribute to the activation of reproductive behavior, including aggression. We investigated here in pied flycatcher (Ficedula hypoleuca) the relationships among territorial aggression, plasma T, and brain AA at the peak of the reproductive season. In a first experiment, blood samples were collected from unpaired males holding a primary territory and, 1 or 2 days later, their aggressive behavior was quantified during standardized simulated territorial intrusions. No relationship was found between individual differences in aggressive behavior and plasma T or dihydrotestosterone levels but a significant negative correlation was observed between number of attacks and plasma corticosterone. In a second experiment, aggressive behavior was measured during a simulated territorial intrusion in 22 unpaired males holding primary territories. They were then immediately captured and AA was measured in their anterior and posterior diencephalon and in the entire telencephalon. Five males that had attracted a female (who had started egg-laying) were also studied. The paired males were less aggressive and correlatively had a lower AA in the anterior diencephalon but not in the posterior diencephalon and telencephalon than the 22 birds holding a territory before arrival of a female. In these 22 birds, a significant correlation was observed between number of attacks/min displayed during the simulated territorial intrusion and AA in the anterior diencephalon but no correlation was found between these variables in the two other brain areas. Taken together, these data indicate that the level of aggression displayed by males defending their primary territory may be limited by the activity of the preoptic aromatase, but plasma T is not playing an important role in establishing individual differences in aggression. Alternatively, it is also possible that brain AA is rapidly affected by agonistic interactions and additional work should be carried out to determine whether the correlation observed between brain AA and aggressive behavior is the result of an effect of the enzyme on behavior or vice versa. In any case, the present data show that preoptic AA can change quite rapidly during the reproductive cycle (within a few days after arrival of the female) indicating that this enzymatic activity is able to regulate rapid behavioral transitions during the reproductive cycle in this species.

Aggression↗