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PubMed2005

Differential effects of past-year stimulant and sedative drug use on alcohol-related aggression.

The goals of this study were to determine the effects of past-year stimulant and sedative drug use on alcohol-related aggression and to examine whether the relation between stimulant drug use and intoxicated aggression is better accounted for by behavioral disinhibition. Participants were 330 healthy social drinkers (164 men and 166 women) between 21 and 35 years of age. Past-year stimulant and sedative use and behavioral disinhibition were assessed via self-report questionnaires. Following the consumption of either an alcohol or a placebo beverage, participants were tested on a modified version of the Taylor Aggression Paradigm [Taylor, S. (1967). Aggressive behavior and physiological arousal as a function of provocation and the tendency to inhibit aggression. Journal of Personality, 35, 297-310] in which mild electric shocks were received from, and administered to, a fictitious opponent. Aggressive behavior was operationalized as the shock intensities administered to the fictitious opponent under conditions of low and high provocation. Results indicated that alcohol significantly strengthened the relation between stimulant drug use and aggression, but only among men. Behavioral disinhibition did not account for this effect. Regardless of past-year drug use, alcohol did not facilitate aggression among women. The present findings suggest that stimulant drug use may be a risk factor for intoxicated aggression for men. However, the underlying mechanisms accounting for this effect remain unclear.

Adult↗
PubMed2007

Amygdala and orbitofrontal reactivity to social threat in individuals with impulsive aggression.

BACKGROUND: Converging evidence from animal and human lesion studies implicates the amygdala and orbitofrontal cortex (OFC) in emotional regulation and aggressive behavior. However, it remains unknown if functional deficits exist in these specific brain regions in clinical populations in which the cardinal symptom is impulsive aggression. We have previously shown that subjects diagnosed with intermittent explosive disorder (IED), a psychiatric disorder characterized by reactive aggressive behavior, perform poorly on facial emotion recognition tasks. In this study we employed a social-emotional probe of amygdala-OFC function in individuals with impulsive aggression. METHODS: Ten unmedicated subjects with IED and 10 healthy, matched comparison subjects (HC) underwent functional magnetic resonance imaging while viewing blocks of emotionally salient faces. We compared amygdala and OFC reactivity to faces between IED and HC subjects, and examined the relationship between the extent of activation in these regions and extent of prior history of aggressive behavior. RESULTS: Relative to controls, individuals with IED exhibited exaggerated amygdala reactivity and diminished OFC activation to faces expressing anger. Extent of amygdala and OFC activation to angry faces were differentially related to prior aggressive behavior across subjects. Unlike controls, aggressive subjects failed to demonstrate amygdala-OFC coupling during responses to angry faces. CONCLUSIONS: These findings provide evidence of amygdala-OFC dysfunction in response to an ecologically-valid social threat signal (processing angry faces) in individuals with a history of impulsive aggressive behavior, and further substantiate a link between a dysfunctional cortico-limbic network and aggression.

Adult↗
PubMed2005

Serotonin and aggressive behavior in rodents and nonhuman primates: predispositions and plasticity.

This review analyzes psychosocial and genetic determinants of aggressive behavior in rodents and nonhuman primates and the role of the serotonin (5-HT) system on aggressive behaviors in order to trace possible evolutionary common origins between psychopathological and adaptive forms of aggression. Studies in primates suggest that deficit in serotonin activity, as indicated by the levels of the cerebrospinal fluid (CSF) serotonin major metabolite 5-hydroxyindoleacetic acid (5-HIAA) correlates with impulsive and aggressive behavior. It is possible that CSF 5-HIAA reflects the prevailing serotonergic tone and may be related to an aggressive trait. Superimposed on this tone are phasic serotonin changes that may be related to the inhibition of aggressive acts. Genetic factors determine aggressive behaviors as demonstrated by classic selection and strain comparison studies. Manipulations of genes targeting 5-HT receptors, transporters and enzymes can influence aggression. Some of these genes related to the serotonin transporter (5-HTT) and the monoamine oxidase A (MAO-A) show a polymorphism that may predispose, under specific environmental conditions, certain individuals to display pathological forms of aggression.

Aggression↗
PubMed2006

Apolipoprotein A-I/apolipoprotein B ratio and aggression in violent and nonviolent young adult males.

Epidemiological, clinical, and experimental studies have linked low or lowered cholesterol levels to aggressive behavior. However, no study has measured the relationship between aggression and apolipoprotein A-I/apolipoprotein B ratio, a robust indicator of cardiac risk. Plasma levels of total cholesterol, HDL-C, LDL-C, triglycerides, apolipoprotein A-I, and apolipoprotein B were measured and correlated with Aggression Questionnaire ratings in 20 young adult males with personality disorders and/or a high propensity toward aggressive behavior and in 40 control subjects. Compared with the control subjects, the subjects in the aggressive group had lower levels of apo A-I and a lower apo A-I/apo B ratio. Whereas in the control subjects, higher levels of aggression were correlated with lower levels of atherogenic lipoproteins (LDL-C and apo B), in the aggressive subjects higher levels of aggression were correlated with lower levels of anti-atherogenic lipoproteins (HDL-C and apo A-I) and higher levels of LDL-C. The results of this study confirm the existence of a relationship between blood lipids and aggressive behavior in young adult males and suggest that the apo A-I/apo B ratio might be an additional marker in the search for biological correlates of increased risk of violence.

Adult↗
PubMed2005

Pleiotropic contributions of nitric oxide to aggressive behavior.

Male mice with targeted deletion of the genes encoding the neuronal (NOS-1-/- or nNOS-/-) isoform of nitric oxide synthase display altered aggressive behaviors. Male nNOS-1-/- mice are more aggressive than wild-type (WT) mice in all testing paradigms. Testosterone is necessary, but not sufficient, for evoking the persistent aggression, and that serotonin (5-HT) metabolism is altered in male nNOS-1-/- mice. The specific deletion of the nNOS-1 gene not only results in a lack of nNOS-1 protein, but in common with many genes, affects several 'down-stream' processes. In this review, we address whether the elevated aggression in male nNOS-1-/- mice reflects pleiotropic effects of the nNOS-1 gene on pain sensitivity, 'anxiety-like', or 'depressive-like' behaviors. For example, male nNOS-1-/- mice display increased sensitivity to painful stimuli, which may prolong aggressive interactions. Despite elevated corticosterone concentrations, nNOS-1 knockout mice appear to be less 'anxious' or fearful than WT mice. Male nNOS-1-/- mice display longer latencies to right themselves on an inverted platform and spend more time in the center of an open field than WT mice. Because of reduced serotonin turnover, the excessive aggressiveness displayed by nNOS-1-/- mice may be symptomatic of a depressive-like syndrome. However, nNOS-1-/- mice rarely display behavioral 'despair' when assessed with the Porsolt forced swim test; rather, nNOS-1-/- mice show vigorous swimming throughout the assessment suggesting that the aggressive behavior does not represent depressive-like behavior. Importantly, aggressive behavior is not a unitary process, but is the result of complex interactions among several physiological, motivational, and behavioral systems, with contributions from the social as well as the physical environment. Lastly, the multiple, and often unanticipated, effects of targeted gene disruption on aggressive behavior are considered.

Aggression↗
PubMed2006

Serotonin-1A receptor activity and expression modulate adolescent anabolic/androgenic steroid-induced aggression in hamsters.

Repeated high dose (5.0 mg/kg) anabolic/androgenic steroid exposure during adolescence stimulates offensive aggression in male Syrian hamsters. These studies examined whether anabolic/androgenic steroid-induced aggression was regulated by the activity and expression of serotonin (5HT) type-1A receptors. In a first experiment, adolescent male hamsters were treated with a mixture of anabolic/androgenic steroids and then scored for offensive aggression in the absence or presence of the selective 5HT1A receptor agonist R(+)-8-OH-DPAT (0.1-0.6 mg/kg). Adolescent anabolic/androgenic steroid-treated hamsters displayed high levels of offensive aggression that could be reversed by enhancing the activity of 5HT1A receptors. The agonist R(+)-8-OH-DPAT dose-dependently reduced the steroid-induced aggressive response, with significant reductions in aggression observed at 0.1-0.3 mg/kg. In a second set of experiments, adolescent hamsters were administered anabolic/androgenic steroids or vehicle and then examined for 5HT1A receptor localization and expression in regions of the brain important for aggression control. Hamsters treated with anabolic/androgenic steroids showed significant decreases in 5HT1A receptor-immunoreactive staining and protein levels in the anterior hypothalamus (i.e., a brain region central to the control of offensive aggression in hamsters) with no concomitant decrease in the number of 5HT1A receptor-expressing neurons. Together, these data support a role for site-specific down-regulation of 5HT1A receptor activity in adolescent anabolic/androgenic steroid-induced aggression.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2004

Intensity of aggressive interactions modulates testosterone in male marmosets.

Androgen is associated with the expression of male-typical behavior, including aggressive behavior, but high levels of androgen may be incompatible with other behavioral systems, such as paternal care. In a variety of species of birds that display paternal care, testosterone (T) levels in males are maintained at low levels, and these levels rise only in response to direct agonistic challenges. This idea has not been thoroughly studied in mammals with biparental care, and we exposed male marmosets (Callithrix kuhlii), a monogamous and biparental primate to aggressive interactions with unfamiliar intruders. Urinary levels of T and cortisol (CORT) were monitored prior to and following these interactions. Baseline T was not correlated with variation in aggression in either residents or intruders, and CORT was not affected by the encounters. However, males responded to an encounter with male intruders with changes in T that correlated with the level of aggression displayed by the resident male during the trial. Encounters with male intruders that elicited high frequencies of aggressive displays by the male resident were associated with increased T 2-6 h and 24 h following the encounter, and encounters that had few aggressive displays resulted in no change or a decrease in T concentrations. Intruders did not demonstrate a significant relationship between T and aggression. Thus, the magnitude of the hormonal response is dependent on the intensity of aggression during a male-male encounter, suggesting that elevated androgens are likely to be a consequence, rather than a cause, of aggressive interactions in marmosets.

Age Factors↗
PubMed2004

Aggressive responding in abstinent heroin addicts: neuroendocrine and personality correlates.

Objective measures of experimentally induced aggressiveness were evaluated in 20 abstinent heroin-dependent subjects, in comparison with 20 normal healthy male subjects. All the subjects were preliminarily submitted to DSM-IV interviews, Buss-Durkee Hostility Inventory (BDHI) and Minnesota Multiphasic Personality Inventory (MMPI II). During a laboratory task, the Point Subtraction Aggression Paradigm (PSAP), subjects earned monetary reinforcers with repeated button presses and were provoked by the subtraction of money, which was attributed to a fictitious other participant. Subjects could respond by ostensibly subtracting money from the fictitious subject (the aggressive response). Money-earning responses were not different in drug-free heroin addicts and controls during the first two sessions and significantly lower during the third session in heroin-dependent subjects (t=2.99, P<.01). Aggressive responses were significantly higher (F=4.9, P<.01) in heroin addicted individuals, in comparison with controls. During the experimentally induced aggressiveness, plasma adrenocorticotropic hormone (ACTH) and cortisol (CORT) concentrations increased less significantly, and norepinephrine (NE) and epinephrine (EPI) levels, together with heart rate (HR), increased more significantly in abstinent heroin-dependent subjects than in healthy subjects. PSAP aggressive responses positively correlated with catecholamine changes, BDHI "direct" and "irritability" scores, MMPI "psychopathic deviate" scores in heroin-dependent subjects and controls, and with CORT responses only in healthy subjects. No correlation was found between heroin-exposure extent (substance abuse history duration) and aggressiveness levels. The present findings suggest that heroin-dependent patients have higher outward-directed aggressiveness than healthy subjects, in relation with monoamine hyperreactivity, after long-term opiate discontinuation. Aggressiveness in heroin addicts seems to be related more to the personality traits than to drug effects. The impairment of hypothalamus-pituitary-adrenal (HPA) axis in abstinent addicted individuals could be due to a long-lasting action exerted by opiates on proopiomelanocortin (POMC) or to a premorbid psychobiological condition, in association with increased sympathetic arousal.

Adrenocorticotropic Hormone↗
PubMed2006

Orbitofrontal correlates of aggression and impulsivity in psychiatric patients.

The association between orbital frontal cortex (OFC) volume and aggression and impulsivity was investigated among a heterogeneous group of non-psychotic psychiatric clients. Fifteen non-psychotic subjects from two different psychiatric clinics (New England Medical Center and Lemuel Shattuck Hospital) with a variety of diagnoses were sequentially referred for magnetic resonance imaging (MRI) for clinical purposes. This convenience sample, clinically stable at the time of evaluation, received a standardized psychiatric diagnostic interview, aggression and impulsivity psychometrics (Barratt Impulsivity, Lifetime History of Aggression, and Buss-Perry Aggression scales), and an MRI protocol with image analysis. OFC gray matter volume, total as well as left and right, was significantly and positively associated with motor impulsivity. OFC asymmetry was associated with aggression, though total, left, and right OFC volume measurements were not. For subjects without affective disorder, there was a strong and positive association of the OFC to motor and no-planning subscales of the Barratt Impulsivity Scale. For subjects with affective disorder, there was a strong association of OFC asymmetry to both of the aggression psychometrics. Consistent with expectation, results are suggestive of OFC involvement in the neural circuitry of impulsivity and aggression. The findings suggest a dissociation of the role of the OFC in relation to aggression and impulsivity, such that the OFC may play a part in the regulation of aggressive behavior and a generative role in impulsive behavior.

Adult↗
PubMed2006

Experimentally induced aggressiveness in heroin-dependent patients treated with buprenorphine: comparison of patients receiving methadone and healthy subjects.

Objective measures of experimentally induced aggressiveness were evaluated in heroin-dependent patients (HDP), 15 receiving buprenorphine (BUP) and 15 receiving methadone (METH) treatment. HDP were randomly assigned to BUP and METH groups. Fifteen healthy subjects (CONT) were included in the study as controls. During a laboratory task, the Point Subtraction Aggression Paradigm, subjects earned monetary reinforcement and could respond by ostensibly subtracting money from a fictitious subject (the aggressive response). Money-earning (points maintained) responses did not differ in BUP patients and in controls. In contrast, point-maintained responses were significantly lower in the group of HDP treated with METH than in both the BUP and CONT groups. Aggressive responses were significantly higher in the HDP group than in the CONT group. No significant differences in aggressive responses were found between the BUP and METH groups. Baseline concentrations of plasma adrenocorticotropic hormone (ACTH) and cortisol (CORT) were higher in HDP than in CONT. During the experimental task, ACTH and CORT increased significantly less in METH patients than in BUP patients and CONT. Norepinephrine (NE) and epinephrine (EPI) levels increased significantly more in HDP than in CONT, without any difference between the METH and BUP patients. PSAP aggressive responses positively correlated with NE and EPI changes, as well as with Buss-Durkee Hostility Inventory (BDHI) scores in both METH and BUP patients and also in CONT subjects. No correlation was found between the extent of heroin exposure, drug doses and aggressiveness levels. BUP, similarly to METH, does not seem to affect outward-directed aggressiveness, as aggressive responses related more to monoamine levels and personality traits than to the action of opioid agonists. Money-earning responses seemed to be unimpaired in BUP patients.

Adrenocorticotropic Hormone↗
PubMed2006

Estrogenic encounters: how interactions between aromatase and the environment modulate aggression.

Initial investigations into the mechanistic basis of aggression focused on the role of testosterone (T) and a variety of studies on non-human animals found that elevated T levels promote aggression. However, many correlational studies have not detected a significant association between aggression and peripheral T levels. One reason for this inconsistency may be due to differential metabolism of T within the brain, in particular, the conversion of T to estrogen by aromatase. Thus, differences in aromatase enzyme activity, estrogen receptor expression, and related cofactors may have important effects on how steroids affect aggressive behavior. Hormone manipulation studies conducted in a wide variety of species indicate that estrogens modulate aggression. There is also growing evidence that social experience has important effects on the production of estrogen within the brain, and some cases can not be explained by androgenic regulation of aromatase. Such changes in central aromatase activity may play an important role in determining how social experiences affect the probability of whether an individual engages in aggressive behavior. Although studies have been conducted in many taxa, there has been relatively little integration between literatures examining aggression in different species. In this review, we compare and contrast studies examining aggression in birds, mammals, and humans. By taking an integrative approach to our review, we consider mechanisms that could explain species differences in how estrogen modulates aggression.

Aggression↗
PubMed2004

The effects of combined aromatase inhibitor and anti-androgen on male territorial aggression in a tropical population of rufous-collared sparrows, Zonotrichia capensis.

Territorial aggression, exhibited by male vertebrates in a reproductive context, is generally thought to be mediated by elevated levels of the gonadal steroid hormone testosterone. Rufous-collared sparrows from Papallacta, Ecuador are only aggressive during the breeding season when plasma testosterone concentrations are elevated. However, previous experiments have determined that during the breeding season testosterone does not increase in response to territorial challenges and testosterone implants do not make males more aggressive. This relationship between testosterone and aggression is different from closely related northern latitude species. We conducted another experiment investigating the role of testosterone in mediating territorial aggression, during the breeding season, in male rufous-collared sparrows. We predicted that blocking the actions of the testosterone would suppress aggression in response to territorial challenges. During the early breeding season males were captured using a simulated territorial intrusion and there was no relationship between time to capture and plasma testosterone, dihydrotestosterone, and corticosterone concentrations. Individual males were then implanted with both the aromatase inhibitor ATD and the anti-androgen Flutamide or empty implants as a control. After one week, birds were challenged with a simulated territorial intrusion and the aggressive responses measured. There were no differences in individual behavioral responses (number of songs, flights, closest approach, or time within 5 m) or overall aggression between the two groups. Androgen levels were elevated, post-implant, in the experimental group suggesting that the treatment was successful by blocking the negative feedback system. We conclude that pharmacologically inhibiting testosterone during the breeding season does not affect territorial aggression in these birds.

Aggression↗
PubMed2004

Behavioral and neuroendocrine correlates of displaced aggression in trout.

In humans and other primates, violent actions performed by victims of aggression are often directed toward an individual or object that is not the source of provocation. This psychological phenomenon is often called displaced aggression. We demonstrate that displaced aggression is either rooted in evolutionarily conserved behavioral and neuroendocrine mechanisms, or represent a convergent pattern that has arisen independently in fish and mammals. Rainbow trout that briefly encountered large, aggressive fish reacted with increased aggression toward smaller individuals. There was a strong negative correlation between received aggression and behavioral change: Individuals subjected to intense aggression were subdued, while moderate assaults induced strong agitation. Patterns of forebrain serotonin turnover and plasma cortisol suggest that the presence of socially subordinate fish had an inhibitory effect on neuroendocrine stress responses. Thus, subordinate individuals may serve as stress-reducing means of aggressive outlet, and displaced aggression toward such individuals appears to be a behavioral stress coping strategy in fishes.

Aggression↗
PubMed2004

Adrenal hormones mediate melatonin-induced increases in aggression in male Siberian hamsters (Phodopus sungorus).

Among the suite of seasonal adaptations displayed by nontropical rodents, some species demonstrate increased territorial aggression in short compared with long day lengths despite basal levels of testosterone. The precise physiological mechanisms mediating seasonal changes in aggression, however, remain largely unknown. The goal of the present study was to examine the role of melatonin, as well as adrenal hormones, in the regulation of seasonal aggression in male Siberian hamsters (Phodopus sungorus). In Experiment 1, male Siberian hamsters received either daily (s.c.) injections of melatonin (15 microg/day) or saline 2 h before lights out for 10 consecutive days. In Experiment 2, hamsters received adrenal demedullations (ADMEDx), whereas in Experiment 3 animals received adrenalectomies (ADx); control animals in both experiments received sham surgeries. Animals in both experiments subsequently received daily injections of melatonin or vehicle as in Experiment 1. Animals in all experiments were tested using a resident-intruder model of aggression. In Experiment 1, exogenous melatonin treatment increased aggression compared with control hamsters. In Experiment 2, ADMEDx had no effect on melatonin-induced aggression. In Experiment 3, the melatonin-induced increase in aggression was significantly attenuated by ADx. Collectively, the results of the present study demonstrate that short day-like patterns of melatonin increase aggression in male Siberian hamsters and suggest that increased aggression is due, in part, to changes in adrenocortical steroids.

Adaptation, Physiological↗
PubMed2006

Low inborn anxiety correlates with high intermale aggression: link to ACTH response and neuronal activation of the hypothalamic paraventricular nucleus.

Aggression constitutes a central problem in several psychopathologies, including anxiety and depression disorders and antisocial behaviors. In particular, the activity of the hypothalamic-pituitary-adrenocortical (HPA) axis has been associated with aggression-related disorders. The present study assessed whether genetically determined levels of anxiety-related behavior influence the level of intermale aggression and whether this is associated with differences in neuroendocrine responsiveness and neuronal activation in the brain. Adult male Wistar rats bred for high (HAB) or low (LAB) anxiety-related behavior were used, as well as non-selected rats (NAB) with an intermediate anxiety level. LAB residents displayed more aggressive behavior than HAB and NAB residents during the resident-intruder (RI) test. Moreover, an inverse correlation was found between the level of anxiety and the level of aggression. The plasma corticotropin (ACTH) response to RI-test exposure was significantly higher in LABs than in HABs and NABs, indicating that a higher level of aggression was linked to an elevated hormonal stress response. Furthermore, LAB residents showed more neuronal activation in the parvocellular part of the hypothalamic paraventricular nucleus (PVN) than HAB residents 1 h after the RI-test. In addition, a tendency toward a higher number of c-Fos-positive cells in LABs compared with HABs was observed in the medial amygdala, hypothalamic attack area and central amygdala, areas relevant for the regulation of aggression. These data demonstrate that low trait anxiety is correlated with high intermale aggression. Furthermore, the increased neuronal activation of the PVN along with the higher ACTH responsiveness might underlie the display of high aggression.

Adrenocorticotropic Hormone↗
PubMed2004

Aggressive driving: an observational study of driver, vehicle, and situational variables.

Over 2000 aggressive driving behaviors were observed over a total of 72 h at six different sites. The behaviors selected for observation were those that are commonly included in "aggressive driving" lists, and they consisted of honking, cutting across one or more lanes in front of other vehicles, and passing on the shoulders. In addition, an exposure sample of 7200 drivers were also observed at the same times and places. Relative risks (RRs) and odds ratios (ODs) were calculated to show the relative likelihood that different drivers under different conditions will commit aggressive behaviors. The rate of aggressive actions observed in this study decreased from the most frequent behavior of cutting across a single lane, through honking, and to the least frequent behaviors of cutting across multiple lanes and passing on the shoulders. Relative to their proportion in the driving population, men were more likely than women to commit aggressive actions, and the differences increased as the severity of the action increased. Drivers who were 45 years old or older were less likely to drive aggressively than younger ones. The presence of passengers was associated with a slight but consistent reduction in aggressive driving of all types; especially honking at other drivers. There was a strong linear association between congestion and the frequency of aggressive behaviors, but it was due to the number of drivers on the road. However, when the value of time was high (as in rush hours), the likelihood of aggressive driving--after adjusting for the number of drivers on the road--was higher than when the value of time was low (during the non-rush weekday or weekend hours). The results have implications for driver behavior modifications and for environmental design.

Adult↗
PubMed2003

Aggression-associated changes in murine olfactory tubercle bioamines.

The relationship between changes in regional brain bioamine levels and the expression of intraspecies aggressive behavior was evaluated in two murine models. In one study, normal male mice were maintained either in aggregate (i.e., normal, intraspecies social behavioral controls) or isolated (i.e., developed, non-social intraspecies aggressive 'fighter' behavior) housing environments, and the accompanying changes in both olfactory tubercle (OT) and hypothalamic (HYPOTH), norepinephrine (NE), dopamine (DA) and serotonin (5-HT) concentration indices quantitated by high-performance liquid chromatography (HPLC) for analysis of behavior-related alterations in localized bioamine deposition loci. Intact mice which had been housed in isolation cages and which exhibited aggressive, intraspecies reflexive-biting ('fighter') behavior when introduced to a novel (stimulus) animal, exhibited significant (P<0.05) elevations in NE levels, and depressed DA concentrations, in the OT regions relative to aggregated controls, indicating an intrinsic social influence on the maintenance of basal adrenergic indices at this neural locus. No changes in 5-HT levels were indicated between control and aggressive, isolated 'fighter' groups in either OT or HYPOTH loci. In addition, the NE and DA levels in the HYPOTH samples of both control and aggressive groups were found to be comparable. In the second study, utilizing an alternate type of aggression-induced murine model, changes in bioamine parameters were determined from samples obtained from aggregated, olfactory-bulbectomized (Obx) mice which are recognized to exhibit an overt, intraspecies, reflexive-biting behavior as compared to sham-operated (control) mice housed under identical conditions. In these studies, Obx-mice exhibited a significant increase in 5-HT levels in the OT relative to sham-operated controls, but similar NE and DA concentrations. In addition, all hypothalamic bioamine indices were found to be comparable between control and Obx groups. These data, collected for both isolation-developed, and experimentally-induced (i.e., OBX), intraspecies aggressive models, indicate that the distinctive types of aggressive behaviors displayed by these two murine models are accompanied by specific alterations in regional bioamine levels within the OT of these groups, relative to controls. These data suggest that the specific type of overt aggressive behavior demonstrated by these models may be causally related to the identified changes in bioamine concentrations in the forebrain regions of the CNS, in loci recognized to participate in environmental recognition and social processing activities.

Aggression↗
PubMed2003

Glutamic acid decarboxylase (GAD65) immunoreactivity in brains of aggressive, adolescent anabolic steroid-treated hamsters.

Chronic anabolic-androgenic steroid (AAS) treatment during adolescence facilitates offensive aggression in male Syrian hamsters (Mesocricetus auratus). The current study assessed whether adolescent AAS exposure influenced the immunohistochemical localization of glutamic acid decarboxylase (GAD65), the rate-limiting enzyme in the synthesis of gamma-aminobutyric acid (GABA), in areas of hamster brain implicated in aggressive behavior. Hamsters were administered high dose AAS throughout adolescence, scored for offensive aggression, and then examined for differences in GAD65 puncta to regions of the hamster brain important for aggression. When compared with control animals, aggressive AAS-treated hamsters showed significant increases in the area covered by GAD65 immunoreactive puncta in several of these aggression regions, including the anterior hypothalamus, ventrolateral hypothalamus, and medial amygdala. Conversely, aggressive AAS-treated hamsters showed a significant decrease in GAD65-ir puncta in the lateral septum when compared with oil-treated controls. However, no differences in GAD65 puncta were found in other aggression areas, such as the bed nucleus of the stria terminalis and central amygdala. Together, these results support a role for altered GAD65 synthesis and function in adolescent AAS-facilitated offensive aggression.

Aggression↗