Resident-intruder Aggression Tests Research Articles

Celastrus paniculatus oil ameliorates synaptic plasticity in a rat model of attention deficit hyperactivity disorder

Objective: To explore the effect and mechanism of action of Celastrus paniculatus oil on the treatment of perinatal rats with attention deficit hyperactivity disorder. Methods: In the perinatal stage, the rats were either isolated or administered with lead acetate to establish an animal model of attention deficit hyperactivity disorder. Atomoxetine served as the reference standard. Animals’ behaviours were assessed through Y-maze, novel object preference, fear conditioning and resident-intruder aggression tests. Oxidative stress parameters, bioamine concentration (dopamine, noradrenaline and 5-hydroxytryptamine), nerve growth factor, interleukin-6, nuclear factor-κB, and tumour necrosis factor (TNF)-α were estimated. Synaptophysin immunohistochemical assay was performed. Results: Celastrus paniculatus oil significantly improved behavioural parameters in Y maze, novel object preference, discrimination index, fear conditioning and resident intruder aggressive tests. The treatment groups showed a decrease in malondialdehyde level. Changes in the levels of dopamine, noradrenaline, and serotonin were restored by Celastrus paniculatus oil. Celastrus paniculatus oil increased nerve growth factor and decreased interleukin-6, nuclear factor-κB, and TNF-α. Synaptophysin immunoreactivity was also improved by Celastrus paniculatus oil with alleviated reactive gliosis, degeneration, and vascular proliferation. Conclusions: This research shows the therapeutic potential of Celastrus paniculatus oil for the treatment of attention deficit hyperactivity disorder.

GluD1 knockout mice with a pure C57BL/6N background show impaired fear memory, social interaction, and enhanced depressive-like behavior.

The GluD1 gene is associated with susceptibility for schizophrenia, autism, depression, and bipolar disorder. However, the function of GluD1 and how it is involved in these conditions remain elusive. In this study, we generated a Grid1 gene-knockout (GluD1-KO) mouse line with a pure C57BL/6N genetic background and performed several behavioral analyses. Compared to a control group, GluD1-KO mice showed no significant anxiety-related behavioral differences, evaluated using behavior in an open field, elevated plus maze, a light-dark transition test, the resident-intruder test of aggression and sensorimotor gating evaluated by the prepulse inhibition test. However, GluD1-KO mice showed (1) higher locomotor activity in the open field, (2) decreased sociability and social novelty preference in the three-chambered social interaction test, (3) impaired memory in contextual, but not cued fear conditioning tests, and (4) enhanced depressive-like behavior in a forced swim test. Pharmacological studies revealed that enhanced depressive-like behavior in GluD1-KO mice was restored by the serotonin reuptake inhibitors imipramine and fluoxetine, but not the norepinephrine transporter inhibitor desipramine. In addition, biochemical analysis revealed no significant difference in protein expression levels, such as other glutamate receptors in the synaptosome and postsynaptic densities prepared from the frontal cortex and the hippocampus. These results suggest that GluD1 plays critical roles in fear memory, sociability, and depressive-like behavior.

The effect of aggression I: The increases of metabolic cost and mobilization of fat reserves in male striped hamsters

Aggression can benefit individuals by enhancing their dominance and thereby their ability to acquire and retain resources that increase survival or fitness. Engaging in aggressive behavior costs energy and how animals manage their energy budget to accommodate aggression remains unclear. We conducted three experiments to examine changes in physiological, behavioral and hormonal markers indicative of energy budget in male striped hamsters subject to resident-intruder aggression tests. Body temperature, metabolic rate and serum corticosterone levels significantly increased in resident hamsters immediately after the introduction of intruders. Energy intake did not change, but the metabolic rate of residents increased by 16.1% after 42-days of repeated encounters with intruders. Residents had significantly decreased body fat content and serum thyroxine (T4) levels, and a considerably elevated tri-iodothyronine (T3)/T4 ratio compared to a control group that had no intruders. Attack latency considerably shortened, and the number of attack bouts and total duration of attacks, significantly increased in residents on day 42 compared to day 1 of experiments. These findings may suggest that the conversion of T4 to T3 is involved in defensive aggression behavior. The mobilization of fat reserves resulting in lean body mass is probably common response to the increased metabolic cost of aggression in small mammals. Aggressive behavior, which is important for the successful acquisition and defense of resources, may be of significance for adaptation and evolution of metabolic rate.

Antistress effects of Kampo medicine "Yokukansan" via regulation of orexin secretion.

ObjectiveVarious stressors induce stress responses through the hypothalamic–pituitary–adrenal and the sympathetic–adrenal–medullary axes, which are regulated, in part, by orexin. For example, secretion of orexin in the hypothalamus is increased in rats exposed to the stress of social isolation for 1 week. In this study, the antistress effects of Kampo medicine Yokukansan (YKS) via the regulation of orexin secretion were investigated using a rat model.Methods and resultsThe administration of 300 mg/kg per day of YKS to rats for 1 week significantly decreased the plasma orexin levels compared with non-treated rats, whereas the administration of 1,000 mg/kg of YKS had no effect on orexin levels. Therefore, 300 mg/kg of YKS was an effective dose for controlling orexin secretion. Subsequently, rats were divided into group-housed control (Con), individually housed stress (Stress), and individually housed YKS (300 mg/kg)-treated stress (Stress + YKS) groups. After 1 week, a resident–intruder aggression test was performed, and the plasma levels of orexin and corticosterone were measured. In the Stress group, aggressive behavior and the levels of corticosterone and orexin significantly increased compared with the Con group; however, these effects were inhibited in the Stress + YKS group. Further, an orexin receptor antagonist (TCS 1102; 10 mg/kg) was intraperitoneally administered to rats exposed to isolation stress to determine whether orexin was involved in stress responses. Under these conditions, aggressive behavior and the level of corticosterone significantly decreased compared with the Stress group.ConclusionThese results suggest that orexin is involved in the control of stress response and that YKS exerts an antistress effect via the regulation of orexin secretion.

Decreased aggression and increased repetitive behavior in Pten haploinsufficient mice.

Aggression is an aspect of social behavior that can be elevated in some individuals with autism spectrum disorder (ASD) and a concern for peers and caregivers. Mutations in Phosphatase and tensin homolog (PTEN), one of several ASD risk factors encoding negative regulators of the PI3K-Akt-mTOR pathway, have been reported in individuals with ASD and comorbid macrocephaly. We previously showed that a mouse model of Pten germline haploinsufficiency (Pten(+/-) ) has selective deficits, primarily in social behavior, along with broad overgrowth of the brain. Here, we further examine the social behavior of Pten(+/-) male mice in the resident-intruder test of aggression, using a comprehensive behavioral analysis to obtain an overall picture of the agonistic, non-agonistic and non-social behavior patterns of Pten(+/-) mice during a free interaction with a novel conspecific. Pten(+/-) male mice were involved in less aggression than their wild-type littermates. Pten(+/-) mice also performed less social investigation, including anogenital investigation and approaching and/or attending to the intruder, which is consistent with our previous finding of decreased sociability in the social approach test. In contrast to these decreases in social behaviors, Pten(+/-) mice showed increased digging. In summary, we report decreased aggression and increased repetitive behavior in Pten(+/-) mice, thus extending our characterization of this model of an ASD risk factor that features brain overgrowth and social deficits.

Dietary arginine depletion reduces depressive-like responses in male, but not female, mice

Previous behavioral studies have manipulated nitric oxide (NO) production either by pharmacological inhibition of its synthetic enzyme, nitric oxide synthase (NOS), or by deletion of the genes that code for NOS. However manipulation of dietary intake of the NO precursor, l-arginine, has been understudied in regard to behavioral regulation. l-Arginine is a common amino acid present in many mammalian diets and is essential during development. In the brain l-arginine is converted into NO and citrulline by the enzyme, neuronal NOS (nNOS). In Experiment 1, paired mice were fed a diet comprised either of an l-arginine-depleted, l-arginine-supplemented, or standard level of l-arginine during pregnancy. Offspring were continuously fed the same diets and were tested in adulthood in elevated plus maze, forced swim, and resident-intruder aggression tests. l-Arginine depletion reduced depressive-like responses in male, but not female, mice and failed to significantly alter anxiety-like or aggressive behaviors. Arginine depletion throughout life reduced body mass overall and eliminated the sex difference in body mass. Additionally, arginine depletion significantly increased corticosterone concentrations, which negatively correlated with time spent floating. In Experiment 2, adult mice were fed arginine-defined diets two weeks prior to and during behavioral testing, and again tested in the aforementioned tests. Arginine depletion reduced depressive-like responses in the forced swim test, but did not alter behavior in the elevated plus maze or the resident intruder aggression test. Corticosterone concentrations were not altered by arginine diet manipulation in adulthood. These results indicate that arginine depletion throughout development, as well as during a discrete period during adulthood ameliorates depressive-like responses. These results may yield new insights into the etiology and sex differences of depression.

Activation of extracellular signal-regulated kinases in social behavior circuits during resident-intruder aggression tests

Using a variety of experimental methods, a network of brain areas regulating aggressive behaviors has been identified in several groups of vertebrates. However, aggressive behavior expressed in different contexts is associated with different patterns of activity across hypothalamic and limbic brain regions. Previous studies in rodents demonstrated that short day photoperiods reliably increase both male and female aggression versus long day photoperiods. Here we used immunohistochemistry and western blots to examine the effect of photoperiod on phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK) in male California mice ( Peromyscus californicus) during resident-intruder tests. Phosphorylated ERK (pERK) can alter neuronal activity in the short term and in the long term acts as a transcription factor. In the posterior bed nucleus of the stria terminalis (BNST) males tested in aggression tests had more pERK positive cells when housed in short days but not long days. This result was replicated in western blot analyses from microdissected BNST samples. In the medial amygdala (MEA), immunostaining and western analyses showed that pERK expression also was generally increased in short days. Immunostaining was also used to examine phosphorylation of cyclic AMP response element binding protein (CREB). CREB can be phosphorylated by pERK as well as other kinases and functions primarily as a transcription factor. Intriguingly, aggressive interactions reduced the number of cells stained positive for phosphorylated CREB in the infralimbic cortex, ventral lateral septum and MEA. This effect was observed in mice housed in long days but not short days. Overall, these data suggest that different (but overlapping) networks of aggressive behavior operate under different environmental conditions.

Deletion of N-type Ca2+ Channel Cav2.2 Results in Hyperaggressive Behaviors in Mice

Voltage-dependent N-type Ca(2+) channels play important roles in the regulation of diverse neuronal functions in the brain, but little is known about its role in social aggressive behaviors. Mice lacking the alpha1B subunit (Ca(v)2.2) of N-type Ca(2+) channels showed markedly enhanced aggressive behaviors to an intruder mouse in the resident-intruder test. The dorsal raphe nucleus (DRN), which contains serotonin neurons, is known to be involved in aggression in animals. We thus examined the DRN neurons in the Ca(v)2.2-deficient (Ca(v)2.2(-/-)) mice. Microinjection of omega-conotoxin GVIA, an N-type Ca(2+) channel-specific blocker, into the DRN of wild type mice resulted in escalated aggression, mimicking the phenotypes of Ca(v)2.2(-/-). Electrophysiological analysis showed increased firing activity of serotonin neurons with a reduced inhibitory neurotransmission in the Ca(v)2.2(-/-) DRN. Ca(v)2.2(-/-) mice showed an elevated level of arginine vasopressin, an aggression-related hormone, in the cerebrospinal fluid. In addition, Ca(v)2.2(-/-) mice showed an increase of serotonin in the hypothalamus. These results suggest that N-type Ca(2+) channels at the DRN have a key role in the control of aggression.

Manipulations of vasopressin alter aggression differently across testing conditions in monogamous and non-monogamousPeromyscus mice

Differences in the distribution of arginine vasopressin (AVP) and a subtype of AVP receptors, the V1a receptor, may explain dissimilarities in social behavior of monogamous and non-monogamous rodents. Intracerebroventricular infusions of AVP and a V1a antagonist were used in sexually naive males of two mouse species, the monogamous and highly aggressive California mouse (Peromyscus californicus) and the non-monogamous and less aggressive white-footed mouse (P. leucopus), to begin testing the interaction between the social system of a species and the effects of AVP on aggression. Two testing conditions, the resident-intruder aggression test (R-I) and the neutral arena aggression test, were used because they may differ in function and underlying biological mechanisms. In the R-I test, administration of the antagonist lengthened attack latencies in California mice. In contrast, blocking V1a receptors did not alter attack latencies in the R-I test in white-footed mice or in the neutral arena aggression test in both species. AVP also did not alter aggression in either species in either behavioral test. Overall, these results suggest that AVP may be more likely to be associated with offensive aggression as measured in the R-I test than with neutral arena aggression and that the effects of AVP manipulations may differ between monogamous and non-monogamous rodents. Aggress. Behav. 31:000–000, 2005. © 2005 Wiley-Liss, Inc.

Testosterone enhances aggression of wild-type mice but not those deficient in type I 5α-reductase

Testosterone’s (T) aggression-enhancing effects may be mediated in part by its 5α-reduced, 3-hydroxysteroid dehydrogenized metabolite 5α-androstane-3α,17β-diol (3α-diol). To test this hypothesis, in Expt. 1 gonadectomized (gdx) C21 mice were administered T, 3α-diol, or vehicle and were observed in the resident intruder test of aggression 1 h later. C21 mice administered androgens had significantly higher incidences of aggression than did vehicle-administered mice. In Expt. 2, wild-type mice and mice deficient in the 5α-reductase type I enzyme were administered T or vehicle and tested 1 h later in the resident intruder paradigm. Wild-type mice administered T had significantly shorter latencies and greater incidences of aggression than did 5α-reductase type I knockout mice administered T or vehicle-administered mice. Data from Expt. 1 are consistent with T and 3α-diol having similar aggression-enhancing effects, and results of Expt. 2 suggest that the inability to metabolize T to its 5α-reduced products may attenuate some aggression-enhancing effects of mice in the resident intruder test of aggression.

Vasopressin and Aggression in Cross-Fostered California Mice (Peromyscus californicus) and White-Footed Mice (Peromyscus leucopus)

To examine how developmental experiences alter neural pathways associated with adult social behavior, we cross-fostered pups between the more aggressive and monogamous California mouse (Peromyscus californicus) and the less aggressive and polygamous white-footed mouse (P. leucopus). Cross-fostered males became more like their foster parents when tested as adults. Male white-footed mice became more aggressive only in an aggression test in a neutral arena, whereas the territorial California mice became less aggressive in resident–intruder aggression test, as measured by attack latency. Only the species that displayed a change in resident–intruder aggression showed a change in arginine vasopressin (AVP) levels: cross-fostered California mice had significantly lower levels of AVP-immunoreactive (AVP-ir) staining than controls in the bed nucleus of the stria terminalis (BNST) and the supraoptic nucleus (SON) and a nonsignificant trend toward lower levels in the medial amygdala (MA). Neither species showed changes in AVP-ir staining in a control area, the paraventricular nucleus (PVN). The changes in AVP-ir staining in the BNST and SON may not be caused by stress because cross-fostering was not associated with changes in adult plasma concentrations of two steroid hormones, corticosterone and testosterone, that have been associated with stress-related alterations in AVP pathways. These results suggest that manipulating the early parental environment can directly alter both a neurotransmitter system and species-typical patterns of social behavior, but that these effects may vary between species and under different social contexts.

Roles of estrogen receptor-alpha gene expression in reproduction-related behaviors in female mice.

The role of gene expression of the estrogen receptor-alpha form (ER alpha) in the regulation of female reproductive behavior was investigated in estrogen receptor knockout (ERKO) mice, deficient specifically for the ER alpha, but not the ER beta, gene. Estrogen- or estrogen- plus progesterone-treated gonadectomized ERKO mice did not show any lordosis response. Detailed behavioral analysis revealed that ERKO females were also deficient in sexual behavioral interactions preceding the lordosis response. They were extremely rejective toward attempted mounts by stud male mice, which could not show any intromissions. During resident-intruder aggression tests, gonadally intact ERKO females were more aggressive toward female intruder mice than wild-type (WT) mice. Gonadectomy did not influence the levels of aggressive behavior, and their genotype differences when mice were tested both before and after gonadectomy. However, when mice were tested after gonadectomy for the first time, very few ERKO mice showed aggression. In contrast to aggression, male-type sexual behavior shown by resident mice toward female intruder mice during aggression tests was not different between ERKO and WT mice and was completely abolished after gonadectomy of the resident mice. Finally, it was also found that ERKO females showed greatly reduced levels of parental behavior toward newborn pups placed in their home cage. These changes in parental behavior were not influenced by gonadectomy. ERKO females retrieved significantly fewer numbers of pups with longer latencies compared with wild-type (WT) or heterozygous (HZ) littermates when they were tested as gonadally intact or 20-65 days after gonadectomy. In addition, during parental behavior tests, a significantly higher percentage of ERKO mice exhibited infanticide compared with WT and HZ mice, which rarely showed infanticide. Taken together, these findings suggest that ER alpha gene expression plays a key role in female mice, not only for sexual behavior but also for other interrelated behaviors, such as parental and aggressive behaviors. In addition, persistence of genotype differences in parental and aggressive behavior after gonadectomy indicates that ER alpha activation during neural developmental processes may also be involved in the regulation of these behaviors.

Behavioural characterization and amounts of brain monoamines and their metabolites in mice lacking histamine H1 receptors

Behavioural assessments were made of mutant mice lacking histamine H1 receptors to reveal the function of H1 receptors in the behaviour of mice. Exploratory behaviour of mice in a new environment was examined to discover whether the absence of H1 receptors in mice affects actions relating to their emotions. The H1 receptor-deficient mice showed a significant decrease in ambulation in an open field and on an activity wheel. Cognitive functions and anxiety were examined using passive avoidance response test and the elevated plus-maze test, respectively. The passive avoidance test did not show any change in latency. The elevated plus-maze test revealed that the transfer latency of the mutant mice was significantly prolonged, indicating that H1 receptors are partly associated with the control of anxiety. Aggressive behaviour was examined by a resident-intruder aggression test. When confronted with an intruder, the mutant mice attacked the intruder significantly slower and less frequently than did wild-type mice after a six-month isolation period. A formalin test and a forced swimming test were used to evaluate the nociceptive response and depressive or despairing state, respectively, of both groups. The mutant mice showed a significant decrease of nociceptive response in the late phase without affecting the early phase. There was no significant difference in the forced swimming test between the two groups. The brain content of monoamines and their metabolites was measured in the H1 receptor null and wild-type mice. The turnover rate of 5-hydroxytryptamine defined by the ratio of 5-hydroxyindoleacetic acid and 5-hydroxytryptamine was significantly increased in the cerebral cortex and hippocampus of H1 receptor null mice. These results support the previous pharmacological findings that histamine modulates various neurophysiological functions such as locomotor activity, emotion, memory and learning, nociception and aggressive behaviour through H1 receptors.

Targeting disruption of histamine H 1 receptors in mice: Behavioral and neurochemical characterization

With gene targeting, one can practically knock out a gene in vivo and creat a mutant organism that completely lacks the gene product. The mutant mice lacking histamine H 1 receptors was generated by the method of gene targeting. In brains of homozygous mutant mice, no specific binding of [ 3H]pyrilamine was seen. The mutant mice showed impaired locomotor activity and exploratory behavior in an open field and activity wheel. Behaviors of the mutant mice were examined with several other tasks such as passive avoidance test, resident-intruder aggression test and formalin test to clarify the role for the H 1 receptors in behaviors. Behavioral changes observed in the mutant mice are almost compatible with those obtained by the classical pharmacological tools. In correlation to the behavioral changes in the mutant mice, 5-hydroxytryptamine release was significantly increased in the brains of mutant mice.

Gonadal Hormones and Aggression‐Maintaining Effect of Alcohol in Male Transgenic Transforming Growth Factor‐α Mice

We have characterized a new transgenic mouse model that offers the unique opportunity to study the biological mechanisms linking aggression to alcohol. In contrast to all other aggressive animal models, the male transgenic mice that overexpress transforming growth factor-alpha (TGF-alpha) maintain their highly elevated aggressive behavior following an alcohol administration. The transgenic mice also exhibit elevated plasma levels of 17 beta-estradiol (E2). Animal data support the role of E2 in aggression and alcohol intake in males. Further, type 2 alcoholism is male-limited, suggesting that gonadal hormones are important. We examined whether gonadal hormones play a role in the resistance to respond to alcohol in the resident-intruder test of aggression among the male transgenic TGF-alpha mice. As previously reported, alcohol had a biphasic effect on sham-operated, nontransgenic controls: 0.6 g/kg increased and 2.0 g/kg inhibited their aggressiveness. Alcohol did not significantly reduce the high levels of aggression in the sham-operated TGF-alpha mice. Castration abolished the difference in aggressive behavior between the transgenic and nontransgenic male mice by reducing aggression. Alcohol did not increase aggressive behavior in these mice. Treatment with pellets releasing 0.25 mg E2 over a 60-day period increased aggression in the castrated male TGF-alpha mice and nontransgenic controls to the levels seen in intact male transgenic mice. Alcohol did not significantly alter aggressive behavior in the E2-treated castrated mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Injection of vehicle is not a stressor in Porsolt's swim test

A single injection or chronic injections with vehicle are reported to induce physical changes in the brain, suggesting this treatment may be stressful. Furthermore, preliminary observations indicate that vehicle injections may interact with the behavioral effects of psychoactive compounds. We investigated the behavioral response to an injection in two tests sensitive to stress: Porsolt's swim test of depressive behavior and the resident-intruder test of aggression. Acute or repeated injections of vehicle did not alter immobility in the swim test in “normal” male NIH Swiss mice, isolated mice, or mice previously exposed to continuous fight stress. Behavior in the resident-intruder test was similar in injected and noninjected mice. The present data suggest that in male NIH Swiss mice a vehicle injection does not induce behavioral changes in tests sensitive to stress, although it is shown to alter various physiological parameters indicative of stress.

The role of body weight in resident-intruder aggression

The behavior of male NIH Swiss mice of various body weights in the resident-intruder test of aggression was investigated. Mice were housed individually for 10 days prior to the test, and allocated to six groups. In the first three groups body weights of residents and group-housed intruders were matched, and the animals were divided into light, average, or heavy groups. In the last three groups weights of the intruder mice were either matched with the residents, or intruders were lighter or heavier than the residents. We found that light residents spent significantly less time in aggressive behaviors and longer time in defensive behaviors than the other two groups. The heavy mice showed most social investigation. The body weights of intruders were also shown to affect the behavior in the test: those residents which had light opponents spent a longer time in aggressive behavior than those which had matched or heavy opponents. The resident mice with heavy opponents showed most defensive behaviors. To study whether pharmacological manipulation may have different effects on behavior in the resident-intruder test in mice having different weights, animals of light, average, and heavy body weight received a low dose (0.8 g/kg) of ethanol 30 min prior to the test. We did not note any effect of ethanol on aggressive behavior in the three groups. The results suggest that body weight plays a significant role in determining the level of aggression and defensive behaviors in the resident-intruder test.

Effects of Tryptophan on Depression and Aggression in STZ-D Mice

Streptozocin-induced diabetic (STZ-D) mice have reduced brain concentrations of tryptophan, a precursor substance for 5-hydroxytryptamine, and show lengthened immobility in Porsolt's swim test, a putative animal model of depression. This study investigated whether tryptophan affects behavior in Porsolt's swim test in STZ-administered male National Institutes of Health Swiss mice. In addition, the effect of tryptophan on behavior in the resident-intruder test of aggression was studied. Tryptophan is effective in the treatment of mild depression and may reduce aggressive behavior. Diabetes was induced with injection of 200 mg/kg body wt i.p. STZ. Two weeks after STZ treatment, the mice received 0, 50, and 100 mg/kg i.p. tryptophan 60 min before the swim test. The STZ-administered mice exhibited lengthened immobility in the swim test, and tryptophan caused a dose-related shortening in their immobility times. The control and STZ mice, which were isolated for 1 wk before the resident-intruder test, did not show any difference in the time spent in social investigation or aggressive or defensive behaviors. However, 100 mg/kg i.p. tryptophan 60 min before the test reduced the social interaction and aggressive behavior of the STZ-D mice but increased these behaviors in controls. Results indicate that tryptophan shortens the increased immobility time and reduces social and aggressive behavior in STZ-D mice. Therefore, the reported reductions in the brain-tryptophan concentrations in STZ-D mice may participate in regulating their behavior.

Blood pressure, heart rate, and regional resistance in behavioral defense

Rats were instrumented with arterial catheters and directional pulsed Doppler flow probes for measurement of arterial blood pressure, heart rate, and blood flow in the renal, mesenteric, and hindquarter vascular beds. When tested as intruders in a resident-intruder aggression test, subjects responded to resident attack with species-characteristic defensive behavior and the “defense reaction” pattern of increased heart rate, renal resistance, and mesenteric resistance, and decreased hindquarter resistance. Blood pressure was variable, but sustained increases in blood pressure were rarely observed. The maintenance of blood pressure during species-specific defensive behavior can be contrasted with the sustained pressor responses observed in the centrally elicited defense reaction. The combination of pulsed Doppler technology and the residentintruder paradigm appears to be a promising method for investigating the mechanisms of cardiovascular adjustment to behavioral defense.