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At least 811 records · Page 45Linked to original sources
PubMed2005

Aggressive behavior increases after termination of chronic sildenafil treatment in mice.

Recent reports to the U.S. Food and Drug Administration Adverse Event Reporting System implicate sildenafil citrate in adverse emotional and aggressive behaviors. Sildenafil citrate (Viagra) is widely prescribed for erectile dysfunction and acts by inhibiting phosphodiesterase Type-5, resulting in accumulation of cyclic-guanosine monophosphate (cGMP). Cyclic-GMP is synthesized by guanylyl cyclase that is directly activated by the messenger molecule, nitric oxide (NO), formed throughout the CNS by the enzyme nitric oxide synthase (NOS). Elevated concentrations of cGMP have been associated with increased aggressive behavior. In addition, the potential effect of cGMP accumulation on NO-mediated behavioral and neuroendocrine function through possible feedback mechanisms remains unspecified; however, neuronal NOS (nNOS) inhibition by pharmacologic agents or ablation of the gene encoding nNOS increases aggressive behavior in male mice. We tested the hypothesis that sildenafil citrate may increase aggression via its actions on cGMP and potential feedback inhibition of NO concentrations. Male C57BL/6 mice were injected with saline vehicle (0), 2, 5, 8, or 10 mg/kg of sildenafil citrate thrice weekly for 4 weeks. Latency to display aggressive behavior, frequency, and duration of aggressive behavior were recorded during neutral-arena aggression tests. No change in agonistic behavior was observed in mice during treatment with sildenafil citrate. However, sildenafil-treated mice given the highest dose were generally more aggressive 1 week post-cessation of drug treatment as compared to vehicle-treated mice. Additional investigation into potential withdrawal effects or abuse doses seems warranted.

Aggression↗
PubMed2005

Serotonin type-1A receptors modulate adolescent, cocaine-induced offensive aggression in hamsters.

Hamsters repeatedly exposed to cocaine throughout adolescence display highly escalated offensive aggression compared to saline-treated littermates. Recently, we have shown that serotonin neural signaling and development play an important role in adolescent cocaine-induced offensive aggression. This study examined whether the adolescent cocaine-induced aggressive response was modulated by serotonin type 1A (5HT1A) receptors. To test this, adolescent male Syrian hamsters were administered cocaine hydrochloride (0.5 mg/kg, i.p.) throughout adolescent development (P27-57) and then tested for offensive aggression after the administration of the 5HT(1A) receptor agonist R(+)-8-OH-DPAT (0.1, 0.3, 0.6, 1.0, 1.25 mg/kg, i.p.). R(+)-8-OH-DPAT dose-dependently reduced cocaine-induced offensive aggression, with a significant reduction observed at 0.3 mg/kg for most of the offensive responses measured. Animals treated with higher doses of R(+)-8-OH-DPAT (0.6-1.25 mg/kg) prior to testing showed significant reductions in all measures of offensive aggression and social interest towards intruders (i.e., contact time), indicating more general behavioral inhibition. Adolescent cocaine-treated animals did not differ in body weight from controls, suggesting that the increased aggression was not due to increased body mass. These data support a role for 5HT1A signaling in adolescent cocaine-induced aggression.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2005

Neonatal handling increases fear and aggression in lactating rats.

Neonatal handling reduces fear in male and cycling female rats, but increases maternal aggressive behavior against intruders to the nest area. Present study aimed to analyze the effects of neonatal handling on the maternal aggressive behavior and the activity in the open field with a predator of lactating rats on the 8th and the 18th postpartum days (periods of high and low aggressiveness). As pups, animals were divided into two groups: nonhandled (no neonatal manipulation) and handled (handling for 1 min during the first 10 days after delivery). As adults, females of both groups were impregnated and tested against a male intruder for aggressive behavior and in the open field with a cat inside a wire-meshed cage. Results showed that on the 8th day frequency of aggressive behaviors of handled females was higher than that of the nonhandled ones, but on the 18th day, no significant difference was detected. Surprisingly, in the open field test, handled females showed decreased locomotion and increased freezing on the 8th day compared to the nonhandled ones. The opposite relationship between increased aggressiveness with reduced fear is observed in the nonhandled control females in early and late lactation periods. However, neonatal handling abolishes this relationship. Apparently, the increased aggressiveness in neonatal handled lactating females does not depend on a decrease in fear. Our findings support the hypothesis that long lasting effects of early life stimulation is a dynamic function depending on the behavioral system and the period of life analyzed. Moreover, they caution the relationship between aggressive behavior and fear.

Age Factors↗
PubMed2006

The effect of buspirone on normal and hypoarousal-driven abnormal aggression in rats.

Aggressiveness is associated with decreased glucocorticoid production, autonomic hypoarousal, and social deficits in antisocial personality disorder and its childhood antecedent conduct disorder. We showed previously that experimentally induced chronic glucocorticoid deficiency leads to abnormal forms of attack, autonomic hypoarousal, and social deficits in rats. We also showed that serotonergic neurotransmission, which downregulates aggressiveness in normal rats appears to lose its aggression-controlling role in glucocorticoid-deficient rats. We suggested that abnormal aggression develops in such rats as a consequence of serotonergic disturbances that result from chronic glucocorticoid deficiency. Here we assessed the effects of the serotonergic anxiolytic buspirone on aggressive behavior in normal and glucocorticoid-deficient rats. Noteworthy, this compound is frequently used in the clinic to control moderate aggression problems. As expected, buspirone dose-dependently reduced the duration of agonistic behaviors in normal rats exposed to resident/intruder conflicts. Similar to earlier experiments, glucocorticoid deficiency dramatically increased the share of attacks directed towards vulnerable body parts of the opponents (head, throat and belly). Surprisingly, 1 and 5 mg/kg buspirone dramatically increased the frequency of biting attacks in glucocorticoid-deficient rats. The share of vulnerable attacks remained as high as in vehicle-treated glucocorticoid-deficient rats. These data show that chronic glucocorticoid deficiency disturbs serotonergic neurotransmission, which reverses the aggression-related effects of the serotonergic agent buspirone. This finding is in line with disparate human findings on the effects of serotonergic agents on aggression in antisocial personality disordered people.

Adrenalectomy↗
PubMed2004

Growth hormone response to clonidine predicts aggression in Alzheimer's disease.

OBJECTIVE: The neurobiology of aggression in Alzheimer's Disease (AD) remains unknown. The objective of this study was to determine if altered central noradrenergic (NE) responsiveness is related to aggression in AD. METHODS: Fifteen institutionalized, non-depressed elderly (11 males, four females, mean age 81.5 +/- 5.5) with probable AD, severe cognitive impairment (MMSE mean 3.3 +/- 4.6) and significant behavioral disturbances (Neuropsychiatric Inventory (NPI) score > or = 8) were studied. Growth Hormone (GH) response to clonidine challenge (5 microg/kg) was used as an index of central alpha(2)-adrenergic function. RESULTS: When patients were divided into those with preserved GH response (GH maximum change from baseline > 0, n = 6) and those with blunted GH response (GH maximum change from baseline < or = 0, n = 9) there were significant differences in levels of aggression as measured by the Cohen-Mansfield Agitation Inventory (CAMI) physical aggression subscale (p = .026). Patients with blunted GH response also had significantly higher levels of aggression against others on the retrospective Overt Aggression Scale (p = 0.027). CONCLUSIONS: Certain types of physically aggressive behaviors are associated with a blunted GH response to clonidine challenge. This finding is consistent with compensatory down-regulation of post-synaptic alpha(2)-adrenergic receptors in response to enhanced NE outflow in aggressive AD patients.

Adrenergic alpha-Agonists↗
PubMed2005

Incidence and clinical correlates of aggression and violence at presentation in patients with first episode psychosis.

This study aimed to identify the incidence and clinical correlates of aggression and violence in first episode psychosis. We prospectively recruited subjects with a first episode of DSM-psychosis presenting from a geographically defined catchment area to a secondary referral psychiatric service over a four-year period (n = 157). We used the Modified Overt Aggression Scale to retrospectively assess aggression (a hostile or destructive mental attitude, including verbal aggression, physical aggression and/or violence) and violence (the exercise of physical force), blind to diagnosis. One in three patients with psychosis was aggressive at the time of presentation. One patient in 14 engaged in violence that caused, or was likely to cause, injury to other people. Aggression was independently associated with drug misuse (odds ratio (OR) 2.80, 95% confidence interval 1.12-6.99) and involuntary admission status (OR = 3.62, 95% CI 1.45-9.01). Violence in the week prior to presentation was associated with drug misuse (OR = 2.75, CI 1.04-7.24) and involuntary admission status (OR = 3.21, CI 1.21-8.50). Violence in the week following presentation was associated with poor insight (OR 2.97, CI 1.03-8.56) and pre-contact violence (OR 3,82, CI 1.34-10.88). In patients with schizophrenia, violence in the week following presentation was associated with drug misuse (OR = 7.81, CI 1.33-45.95) and high psychopathology scores (OR = 20.59, CI 1.66-254.96). Overall, despite a high rate of verbal aggression, physical violence towards other people is uncommon in individuals presenting with first episode psychosis.

Aggression↗
PubMed2004

Activation of aggressive behavior by progesterone and testosterone in male tree lizards, Urosaurus ornatus.

Testosterone is usually thought to be the major sex steroid regulating adult male territorial aggression in vertebrates. However, recent evidence has suggested a role for progesterone, as well as testosterone, in the organization of the two male reproductive phenotypes of tree lizards (Urosaurus ornatus), which differ in adult levels of territorial behavior. In the present experiment we tested whether progesterone and testosterone could also play an activational role in the expression of adult aggressive behavior. We subjected post-reproductive male tree lizards to the following treatments: sham surgery, castration, castration with progesterone supplementation, and castration with testosterone supplementation. We measured several different dimensions of aggressive behavior. Overall in these post-reproductive animals, the level of aggression from lowest to highest was: castrates, shams, progesterone-treated, and testosterone-treated. Although testosterone appears to be the more potent regulator of aggressive behavior, progesterone enhanced several measures of aggression suggesting that it could play a role in natural regulation of aggressive behavior. This initial study used very high levels of progesterone (similar to or above those experienced by hatchlings) to maximize the probability of detecting an effect. Further studies are needed to determine if natural adult progesterone levels are sufficiently high to influence aggressive behavior.

Aggression↗
PubMed2006

Individual differences in estrogen receptor alpha in select brain nuclei are associated with individual differences in aggression.

Steroid hormones play an important role in modulating social behavior in many species. Estrogens are thought to act on an interconnected network of hypothalamic and limbic brain areas to affect aggressive behavior, although the specific nuclei unknown remain unspecified. We show that individual variation in estrogen receptor alpha (ERalpha) immunoreactivity in the lateral septum (LS), ventral bed nucleus of the stria terminalis (vBNST), and anterior hypothalamus (AHA) of CD-1 mice is positively correlated with aggressive behavior. When males were treated with fadrozole (an aromatase inhibitor), aggressive behavior was reduced, although castration did not reduce aggression. These results suggest that estrogens modulate aggressive behavior by acting on a circuit that includes the LS, vBNST, and AHA and that the source of estrogens is non-gonadal. Fadrozole also decreased c-fos expression in the lateral septum following aggressive encounters. Although the effects of estrogen on aggression appear to involve regulation of neuronal activity in the LS, additional processes are likely involved. These results suggest that estrogen acts in a specific subset of a complex network of nuclei to affect aggressive behavior.

Aggression↗
PubMed2006

Physical provocation of pubertal anabolic androgenic steroid exposed male rats elicits aggression towards females.

Human studies suggest that anabolic androgenic steroid (AAS) users are aggressive towards women. This study used a rat model to evaluate whether AAS potentiated aggression towards females and the conditions under which this occurs. Gonadally intact pubertal male rats received one of the following AAS treatments (5 mg/kg s.c. 5 days/week for nine weeks): testosterone (T), stanozolol (S), testosterone + stanozolol (T + S), or vehicle control. Each rat was tested with 3 conspecific stimuli: ovariectomized females (OVX), estrogen only females (E), and estrogen + progesterone females (E + P). The response to physical provocation was tested under three conditions: without physical provocation, provocation of the experimental male, and provocation of the conspecific female. Provocation was a mild tail pinch. Both aggressive and sexual behaviors were measured during each test. In the absence of physical provocation, AAS males were not aggressive towards females. However, provocation significantly increased aggression in males treated with testosterone but only towards OVX females. In the presence of E or E + P females, all animals displayed sex behavior, not aggression. Thus, factors such as the nature of the AAS and the hormonal status of the females are important in determining whether male rats will be aggressive towards females. However, the most salient factor determining aggression towards females is the presence of provocation in combination with high levels of testosterone.

Aggression↗
PubMed2002

Psychological characteristics of aggressive drivers with and without intermittent explosive disorder.

We compared two groups of aggressive drivers, those who met criteria for Intermittent Explosive Disorder (IED) (n=10) and comparable aggressive drivers who did not meet IED criteria (n=20), to a group of non-aggressive driving controls (n=20) on measures of psychological distress, anger, hostility, and Type A behavior as well as measures of aggressive driving and driving anger and their driving records. There were few differences between the aggressive drivers with IED and those without IED. The IED positive aggressive drivers endorsed more assaultiveness and resentment as well as more impatience and showed trends to have more hostility and angry temperament. When all aggressive drivers were compared to controls, differences emerged on anxiety, hostility, and anger as well as on measure specific to aggressive driving (competitiveness) and driving anger (at slow drivers and traffic obstructions).

Adolescent↗
PubMed1997

A further evaluation of the Aggression Questionnaire: issues of validity and reliability.

An analysis of the four scales from Buss and Perry's (1992, Journal of Personality and Social Psychology, 63, 452-459) Aggression Questionnaire was conducted. Examined was the internal consistency, test-retest reliability, the influence of social desirability, and the interrelationships with other measures of aggression. The results suggest that the four scales of The Aggression Questionnaire have moderate to high internal consistencies and are stable over seven months of testing. Social desirability was found to have a moderately high negative relationship with the aggression scales suggesting that social desirability may influence responses provided on The Aggression Questionnaire. In addition, the four aggression scales were found to be positively related to other measures of aggression including scales assessing affect instability and aggressive attitudes, as well as scales designed for clinical use, suggesting some degree of construct validity.

Adolescent↗
PubMed2000

3-bromo-7-nitroindazole, a neuronal nitric oxide synthase inhibitor, impairs maternal aggression and citrulline immunoreactivity in prairie voles.

Lactating female rodents are aggressive against intruders when they are rearing and protecting pups. In prairie voles, Microtus ochrogaster, females exhibit a dramatic increase in citrulline immunoreactivity (citrulline-IR) in the paraventricular nucleus (PVN), but not in control regions of the brain, in association with maternal aggression. Citrulline is an indirect indicator of nitric oxide (NO) synthesis and it is possible that NO release in the PVN is an important element in the control of maternal aggression in prairie voles. In this study, we sought to examine the role of NO in maternal aggression by selectively inhibiting neuronal nitric oxide synthase (nNOS) in lactating prairie voles. Intraperitoneal injections of the nNOS inhibitor, 3-bromo-7-nitroindazole (3-Br-7NI) (20 mg/kg), three time per day over 4 days resulted in significant impairment of the expression of maternal aggression in terms of the average time in aggressive encounters, the average number of attacks, and the average latency to first attack. These behavioral deficiencies were observable beginning two days following the onset of drug treatment. The average time spent sniffing the intruder was indistinguishable between the 3-Br-7NI- and oil-treated females. In 3-Br-7NI-treated relative to oil-treated females, the number of citrulline-positive cells was reduced by 70% in the PVN and by 50% in the anterior amygdaloid area, a control region of the brain. Taken together, these results indicate that 3-Br-7NI effectively inhibits maternal aggression and NO production in prairie voles and suggest that the central release of NO may play an important role in the production of maternal aggression in prairie voles.

Aggression↗
PubMed2003

Castration does not decrease nonreproductive aggression in yearling male European starlings (Sturnus vulgaris).

In the nonbreeding season, some bird species express high levels of aggression despite basal plasma testosterone (T) concentrations. Consequently, nonreproductive aggression is believed to be independent of plasma T. In the present study, we investigated the effect of castration on nonreproductive aggressive behavior in yearling male European starlings (Sturnus vulgaris). We paired castrated (Cx) with control (C) males in dyadic trials during three test periods (December, January-February, and March-April), and by using an infrared camera, we defined which male was the most aggressive one when both males were competing over access to a nest box to roost in. During each of the three periods, Cx males behaved more aggressively than C males but differences between groups did not reach significance. When analyzing the results of the three periods together, Cx males were found to be significantly more aggressive than C males. Likewise, when considering only the second and third period (when plasma T levels of C males were significantly higher than those of Cx males) the same result was obtained. Furthermore, in the third period, aggression tended to be lower than in the first and second period, although T concentrations of C males were highest in this period. Our data thus clearly show that nonreproductive aggression in yearling male starlings is independent of gonadal sex steroids and suggest it even increases by castration.

Aggression↗
PubMed2003

Fluoxetine treatment decreases territorial aggression in a coral reef fish.

Serotonin is an important neurotransmitter in the regulation of social interactions in many animals. Correlative studies in numerous vertebrate species, including fishes, indicate that aggressive males have lower relative serotonergic activity than less aggressive males. We used fluoxetine, a selective serotonin reuptake inhibitor, to experimentally enhance serotonergic neurotransmission in a territorial coral reef fish and test the role of this neurotransmitter in mediating aggressive behavior and dominance interactions. The bluehead wrasse, Thalassoma bifasciatum, has a complex social system in which large males aggressively defend spawning territories from intruders. In separate experiments, we tested the effects of chronic and acute fluoxetine treatments on aggressive behavior using a resident-intruder design. In a laboratory experiment, males treated daily with intraperitoneal fluoxetine injections for 2 weeks (6 microg/g bw) displayed fewer intruder chases than saline-treated controls. Chronically fluoxetine-treated males also showed lower levels of activity than saline controls prior to intruder trials. However, activity was not correlated with chases on an individual level, indicating the lower aggression displayed by fluoxetine-treated males was not due solely to general reductions in behavioral display. A field study exposed males to a confined territorial intruder following single intraperitoneal injections of fluoxetine (10 microg/g bw) or saline given to the same individual on different days. The frequency of aggressive chases following acute fluoxetine treatment was significantly lower than that following saline injections. This study experimentally supports the link between serotonin and aggressive behavior in fishes in both a controlled laboratory testing environment and the animal's natural habitat.

Aggression↗
PubMed1997

Anabolic-androgenic steroid exposure during adolescence and aggressive behavior in golden hamsters.

Anabolic androgenic steroid (AAS) abuse by adolescents represents a significant health care risk due to the potential for long-term negative physical and psychological sequelae, including increased aggressive behavior. The current experiments examined the effects of AAS use in young male adolescent hamsters (Mesocricetus auratus) and their consequences on aggressive behavior. It was hypothesized that AAS administration during adolescence predisposes hamsters to heightened levels of aggressive behavior (i.e., offensive aggression). To test this hypothesis adolescent male hamsters were administered high doses of synthetic AAS to mimic a 'heavy use' self-administration regimen used by athletes. Immediately following the exposure to AAS hamsters were tested for aggressive behavior using a resident-intruder model. Animals treated with high doses of AAS during their adolescent development showed heightened measures of offensive aggression i.e., decreased latency to bite and increased total number of attacks and bites) during the test period, while measures of total activity (total contact time) between the animals remained unchanged. AAS-treated males did not differ in body weight from controls, suggesting that the increased aggression was not due to increased body mass. The results of this study show that exposure to AAS during adolescence facilitates aggressive response patterns, but does not alter body weight.

Aggression↗
PubMed1997

The influence of menstrual-cycle phase on the relationship between testosterone and aggression.

Plasma testosterone levels and aggressive behavior were measured in 12 women with and without perimenstrual affective symptomatology (e.g., depression, irritability) during the menstrual, midfollicular, ovulatory, and premenstrual phases of the menstrual cycle. The Point Subtraction Aggression Paradigm was used to quantify aggressive response to provocation. Subjects had two response options: a point-maintained option (100 presses earned a point worth 10 cents) and an aggressive response option (10 presses ostensibly subtracted a point from a fictitious partner's counter). Subjects were provoked by the periodic subtraction of a point that was attributed to the responding of a fictitious opponent. Although plasma testosterone levels (determined by radioimmunoassay) increased significantly during the ovulatory phase, aggressive response to provocation remained unchanged across the menstrual cycle. Plasma testosterone did not differ between the 2 groups during any phase. A relationship between plasma testosterone levels and use of the aggressive response option was seen only during the midfollicular phase (Spearman r = .673, p = .017). These preliminary data suggest that: 1. The relationship in female subjects between endogenous testosterone and aggressive behavior is inconsistent; 2. self-report of perimenstrual symptomatology is a more consistent predictor of aggressive behavior across the menstrual cycle than plasma testosterone; and 3. perimenstrual emotional symptomatology is not related to testosterone levels.

Adolescent↗
PubMed1981

Sexual dimorphism in the hormonal control of aggressive behavior of rats.

Male and female rats housed together in small groups both became aggressive toward strange rats placed into their cages. However, male rats mainly attack male intruders and female rats mainly attack female intruders. The hormonal requirements for this aggression are also sexually dimorphic. Castration of the male residents causes a decrease in aggressive behavior, but ovariectomy of the female residents has little effect on their aggression. Replacement therapy to castrated males with 500 microgram/day of testosterone propionate (TP) restores all components of aggressive behavior within 2-3 weeks. Replacement therapy with 5 microgram/day of estradiol benzoate for 3 weeks had no effect on castrated males' aggressive behavior, nor did it cause the males to start attacking female intruders. Replacement therapy to ovariectomized females had a quite different effect. Treatment with EB or EB and progesterone reduced or blocked attack toward intruder females but did not alter the low level of attack toward males. Treatment with TP for 3 weeks also slightly reduced attack toward female intruders but increased the probability of attack toward male intruders. The sex-specificity of aggression and the differential influence of hormones suggests that different mechanisms may be responsible for aggression in males and in females.

Aggression↗
PubMed1997

Effects of serotonin 1A or 1B receptor agonists on social aggression in male and female Syrian hamsters.

Numerous studies have demonstrated that activation of serotonin 5-HT1A or 5-HT1B receptor decreases aggression in male mammals. To determine whether female mammals also show decreased aggression in response to 5-HT1A or 5-HT1B activation, we assessed the effects of the serotonin receptor agonists 8-OH-DPAT (5-HT1A) and CGS-12066A (5-HT1B) on aggression in female Syrian hamsters. Female Syrian hamsters were tested for interfemale aggression 2 days before and 15 min after receiving intracerebroventricular infusions of 8-OH-DPAT (5, 10, 20 microg) or CGS-12066A (5, 10, 20 microg). Neither drug affected aggression as measured by the latency and frequency of attacks or uprights, although the highest dose of 8-OH-DPAT increased general activity. For male hamsters, intraventricular infusions of 10 microg of 8-OH-DPAT essentially eliminated aggression, whereas 5 microg of 8-OH-DPAT or 20 microg of CGS-12066A were without effect. Systemic treatment with 8-OH-DPAT (1 mg/kg body weight) did reduce aggression in females, although there was an attendant increase in symptoms of nonspecific serotonergic activity. There were no behavioral effects of systemic CGS-12066A (4 mg/kg body weight) on female hamsters. These results indicate that there may be sex differences in the neurochemical regulation of aggression and point to a need for more studies directed at this issue.

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