Abstract The authors conducted a comprehensive review to understand the relation between personality and aggressive behavior, under provoking and nonprovoking conditions. The qualitative review revealed that some personality variables influenced aggressive behavior under both neutral and provocation conditions, whereas others influenced aggressive behavior only under provocation. Studies that assessed personality variables and that directly measured aggressive behavior were included in the quantitative review. Analyses revealed that trait aggressiveness and trait irritability influenced aggressive behavior under both provoking and neutral conditions but that other personality variables (e.g., trait anger, Type A personality, dissipation-rumination) influenced aggressive behavior only under provoking conditions. The authors discuss possible relations between these patterns of aggressive behavior and the personality dimensions of Agreeableness and Neuroticism and consider implications for theories of aggression.

Abstract Aggression is a common response to provocation, albeit with considerable interindividual differences. In this fMRI study, we investigated emotional reactivity to threat as possible link between provocation and aggression, as well as the neural correlates of this relationship. We hypothesized that emotional reactivity, measured as fear potentiation (FP) of the startle response, would be negatively associated with aggressive behavior and would modulate neural activity during an aggressive interaction. In 30 healthy female participants, FP was measured as the difference between blink amplitudes while watching threatening vs neutral pictures. Participants subsequently engaged in a variant of the Taylor Aggression Paradigm (TAP), while being scanned. During the TAP, participants selected a punishment level for either a highly provoking or a nonprovoking opponent. There was no difference in aggressive behavior between participants high and low in FP. However, we found a negative correlation between FP and the neural provocation effect in several regions of a network previously associated with mentalizing including the medial prefrontal cortex, precuneus and the temporo-parietal junction. Independently of the FP variability, aggressive behavior correlated with the provocation effect on activity in the caudate nucleus. Our results indicate that during a provocative confrontation, high emotional reactivity to threat suppresses recruitment of the mentalizing network. The Author (2013). Published by Oxford University Press. For Permissions, please email: journals.permissions@oup.com.

Altered neural processing of social signals such as angry facial expressions has been associated with increased aggressive , but evidence for this relationship in healthy persons using ecologically valid experimental designs is lacking. We presented socially relevant videos of facial expressions in a functional magnetic resonance imaging (fMRI) version of the well-established Taylor Aggression Paradigm and investigated 41 healthy male participants, of whom 32 were included in the analysis. In each round of this competitive reaction time task, participants observed their opponent while he selected a punishment level for him, bearing either a neutral or angry facial expression. Afterward, participants in turn selected a punishment level for their opponent. Across participants, reactivity of the medial orbitofrontal cortex (OFC) to angry facial expressions was negatively related to aggressive . Within participants and across trials, activity in the anterior cingulate cortex () was positively related to aggressive specifically in response to angry expressions. Moreover, we found an effect of angry expressions on neural activity patterns during later stages of the task, demonstrating that the effect of angry expressions on neural reactivity is more than just a short-lived, stimulus-driven response. Our results underscore the importance of OFC and for the shaping of socially adaptive responses to provocation.

Abstract The basic organization of the catecholamine-containing neuronal systems and their axonal projections in the brain was initially worked out using classical histofluorescence techniques during the 1960s and 1970s. The introduction of more versatile immunohistochemical methods, along with a range of highly sensitive tract-tracing techniques, has provided a progressively more detailed picture, making the dopamine system one of the best known, and most completely mapped, neurotransmitter systems in the brain. The purpose of the present review is to summarize our current knowledge of the diversity and neurochemical features of the nine dopamine-containing neuronal cell groups in the mammalian brain, their distinctive cellular properties, and their ability to regulate their dopaminergic transmitter machinery in response to altered functional demands and aging.

Abstract The goal of this paper is to consider anger from a cognitive neuroscience perspective. Five main claims are made: First, reactive aggression is the ultimate behavioral expression of anger and thus we can begin to understand anger by understanding reactive aggression. Second, neural systems implicated in reactive aggression (amygdala, hypothalamus and periaqueductal gray; the basic threat system) are critically implicated in anger. Factors such as exposure to extreme threat that increase the responsiveness of these systems, should be (and are in the context of Post Traumatic Stress Disorder), associated with increased anger. Third, regions of frontal cortex implicated in regulating the basic threat system, when dysfunctional (e.g., in the context of lesions) should be associated with increased anger. Fourth, frustration occurs when an individual continues to do an action in the expectation of a reward but does not actually receive that reward, and is associated with anger. Individuals who show impairment in the ability to alter behavioral responding when actions no longer receive their expected rewards should be (and are in the context of psychopathy) associated with increased anger. Fifth, someone not doing what another person wants them to do (particularly if this thwarts the person's goal) is frustrating and consequently anger inducing. The response to such a frustrating social event relies on the neural architecture implicated in changing behavioral responses in non-social frustrating situations.

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Conclusions: We developed a platform-independent modeling tool that provides valid and consistent multivariate Granger causality analysis particularly suited for FMRI data. The program identifies patterns of association among brain ROIs that have been identified with

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.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.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.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.

Building on animal and human lesion evidence, neuroimaging studies are increasingly identifying abnormalities in corticolimbic circuits mediating aggressive behavior. This review focuses on three neural systems involved in impulsive/reactive aggression: 1) subcortical neural systems that support the production of aggressive impulses; 2) decision-making circuits and social-emotional information processing circuits that evaluate the consequences of aggressing or not aggressing; and 3) frontoparietal regions that are involved in regulating emotions and impulsive motivational urges. We review psychiatric disorders, including borderline personality disorder and antisocial personality disorder, characterized by elevated reactive aggression, focusing on abnormalities in these three neural systems.

The ability to successfully suppress impulses and angry affect is fundamental to control aggressive reactions following provocations. The aim of this study was to examine neural responses to provocations and aggression using a laboratory model of reactive aggression. We used a novel functional magnetic resonance imaging point-subtraction aggression paradigm in 44 men, of whom 18 were incarcerated violent offenders and 26 were control non-offenders. We measured brain activation following provocations (monetary subtractions), while the subjects had the possibility to behave aggressively or pursue monetary rewards. The violent offenders behaved more aggressively than controls (aggression frequency 150vs84,P=鈥0.03) and showed significantly higher brain reactivity to provocations within the amygdala and striatum, as well as reduced amygdala-prefrontal and striato-prefrontal connectivity. Amygdala reactivity to provocations was positively correlated with task-related behavior in the violent offenders. Across groups, striatal and prefrontal reactivity to provocations was positively associated with trait anger and trait aggression. These results suggest that violent individuals display abnormally high neural sensitivity to social provocations, a sensitivity related to aggressive behavior. These findings provide novel insight into the neural pathways that are sensitive to provocations, which is critical to more effectively shaped interventions that aim to reduce pathological aggressive behavior.

When the landmark patient Phineas Gage died in 1861, no autopsy was performed, but his skull was later recovered. The brain lesion that caused the profound personality changes for which his case became famous has been presumed to have involved the left frontal region, but questions have been raised about the involvement of other regions and about the exact placement of the lesion within the vast frontal territory. Measurements from Gage's skull and modern neuroimaging techniques were used to reconstitute the accident and determine the probable location of the lesion. The damage involved both left and right prefrontal cortices in a pattern that, as confirmed by Gage's modern counterparts, causes a defect in rational decision making and the processing of emotion.

Abstract Here we provide a review of the animal and human literature concerning the role of the amygdala in fear conditioning, considering its potential influence over autonomic and hormonal changes, motor behavior and attentional processes. A stimulus that predicts an aversive outcome will change neural transmission in the amygdala to produce the somatic, autonomic and endocrine signs of fear, as well as increased attention to that stimulus. It is now clear that the amygdala is also involved in learning about positively valenced stimuli as well as spatial and motor learning and this review strives to integrate this additional information. A review of available studies examining the human amygdala covers both lesion and electrical stimulation studies as well as the most recent functional neuroimaging studies. Where appropriate, we attempt to integrate basic information on normal amygdala function with our current understanding of psychiatric disorders, including pathological anxiety.

Abstract Neuropeptides vasopressin and oxytocin regulate a variety of behaviors ranging from maternal and pair bonding to aggression and fear. Their role in modulating fear responses has been widely recognized, but not yet well understood. Animal and human studies indicate the major role of the amygdala in controlling fear and anxiety. The amygdala is involved in detecting threat stimuli and linking them to defensive behaviors. This is accomplished by projections connecting the central nucleus of the amygdala (CeA) to the brain stem and to hypothalamic structures, which organize fear responses. A recent study by Huber et al demonstrates that vasopressin and oxytocin modulate the excitatory inputs into the CeA in opposite manners. Therefore this finding elucidates the mechanisms through which these neuropeptides may control the expression of fear.

The current study examined whether reactive and/or proactive aggression in adolescent males prospectively predicted increased levels of internalizing symptoms (depression and anxiety) in late adolescence. It was postulated that reactive aggression would be robustly related to later internalizing problems, but only among adolescent males who had problematic family or peer social relationships. Participants were a racially diverse group of 289 adolescent males (Mean age65=6516). Measures of reactive and proactive aggression, peer rejection, and poor parent–adolescent communication were examined as predictors of both depression and anxiety symptoms assessed approximately 3 years later. The interactive effects between the two facets of aggression and measures of peer rejection and poor parent–adolescent communication in predicting internalizing problems was also examined. Adolescents with high levels of reactive aggression were more likely to exhibit elevated internalizing problems during late adolescence, even when controlling for pre-existing levels of anxiety/depression. However, this association only emerged for adolescents who had high levels of peer rejection and/or poor communication with their parent. Consistent with expectations, proactive aggression was unrelated to internalizing symptoms regardless of social relationship quality. Adolescent reactive, but not proactive, aggression is a risk factor for the development of internalizing problems. However, the findings suggest that interventions designed to foster positive social relationships among reactively aggressive youth may help protect them from developing significant internalizing problems over time. Aggr. Behav. 40:69–78, 2014. 08 2013 Wiley Periodicals, Inc.

Abstract An important distinction in research on the neural mechanisms of emotion regulation involves the relatively limited duration of emotional states versus emotional traits that are defined as the stable tendency to experience particular emotions in daily life. Neuroimaging investigations of the regulation of anger states point to the involvement of reciprocal changes in the prefrontal cortex and amygdala activity, but the neural substrate of trait anger has received less attention. We used resting-state functional MRI to determine whether the variation in the strength of functional connectivity between the amygdala and the orbitofrontal cortex is associated with trait anger. Sixteen healthy men completed the Spielberger State-Trait Anger Expression Inventory. Correlational analysis for resting-state functional connectivity (RSFC) was carried out with the left and the right amygdala as separate seed regions. Anger measures were correlated to RSFC involving the right and the left amygdala on a voxel-by-voxel basis across all individuals. We found that Trait Anger was inversely associated with the strength of RSFC between the amygdala and the contralateral middle orbitofrontal cortex. The association was stronger for the right amygdala-left orbitofrontal connection. Anger Control, the tendency to try to control expressions of anger, showed the opposite pattern of being positively correlated with amygdala-orbitofrontal connectivity. The present study provides evidence that RSFC in a corticolimbic circuit might subserve stable differences in anger regulation. Our findings also suggest that RSFC may prove valuable as a trait marker for disorders characterized by emotional dysregulation such as depression, anxiety, and personality disorders.

Abstract Lisa M. Gatzke-Kopp and Theodore P. Beauchaine review the evidence for a frontostriatal, dopaminergic deficit in developmental disorders of impulsivity. In particular, they review findings indicating nigrostriatal, mesocortical (cognitive), and mesolimbic (motivational) system deficits in attention-deficit/hyperactivity disorder (ADHD) and conduct disorder (CD). Although the precise mechanism--in terms of hyperactivity or hypoactivity of the dopaminergic system--remains unknown, it appears that each of these functionally integrated systems may contribute to different symptoms observed in the ADHD syndrome. The authors suggest that this complex etiology may result in different patterns of symptoms across individuals diagnosable with ADHD and may necessitate a combined behavioral and neurobiological approach to diagnosis. (PsycINFO Database Record (c) 2012 APA, all rights reserved)

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Abstract The purpose of this study was to evaluate the validity of a modified version of the Taylor Aggression Paradigm (TAP) as a measure of direct physical aggression. Hypotheses were generated from recent theory pertinent to the categorization and measurement of aggressive behavior as well as widely supported effects of alcohol intoxication and gender on aggression. Participants were 328 (163 men and 165 women) healthy social drinkers between 21 and 35 years of age who completed self-report personality inventories designed to assess one's propensity toward direct physical aggression, verbal aggression, trait anger, and hostility. Following the consumption of either an alcohol or a placebo beverage, participants were tested on the TAP, in which mild electric shocks were received from, and administered to, a fictitious opponent during a competitive task. Direct physical aggression was operationalized as the shock intensities (i.e., first trial shock intensity, mean shock intensity, proportion of highest shock) administered to the fictitious opponent. Although all self-report measures were significantly associated with the three TAP indices, the associations involving physical aggression were strongest. In addition, self-report measures of physical aggression consistently predicted higher levels of aggression on the TAP indices in men, compared with women, and in intoxicated, relative to sober, participants. Taken as a whole, this pattern of findings provides further evidence for the validity of the TAP as a measure of direct physical aggression for men and women. Aggr. Behav. 34:214 229, 2008. 2007 Wiley-Liss, Inc.

In this review, we examine the functions of the striatum and the evidence that this brain region may be compromised in antisocial individuals. The striatum is involved in the processing of reward-related information and is thus important in reward-based learning. We review evidence from a growing number of brain imaging studies that have identified differences in the structure or functioning of the striatum either in antisocial groups or in relation to personality traits that are associated with antisocial behavior such as impulsivity and novelty seeking. Evidence from structural imaging studies suggests that the volume of the striatum is increased in antisocial populations, although evidence of localization to specific subregions is inconsistent. Functional imaging studies, which similarly tend to find increased functioning in the striatum, suggest that the striatum is not necessarily hypersensitive to the receipt of reward in antisocial individuals but instead may not be appropriately processing the absence of a reward, resulting in continuous responding to a stimulus that is no longer rewarding. This may impair the ability of individuals to flexibly respond to the environment, thus contributing to impulsivity and antisocial behavior. We conclude by discussing genetic and environmental factors that may affect the development of the striatum.

Investigations into the specific association of amygdala volume, a critical aspect of the fronto-limbic emotional circuitry, and aggression have produced results broadly consistent with the 'larger is more powerful' doctrine. However, recent reports suggest that the ventral and dorsal aspects of the amygdala play functionally specific roles, respectively, in the activation and control of behavior. Therefore, parceling amygdala volume into dorsal and ventral components might prove productive in testing hypotheses regarding volumetric association to aggression, and impulsivity, a related aspect of self-control. We sought to test this hypothesis in a group of 41 psychiatric patients who received standard magnetic resonance imaging and a psychometric protocol including aggression and impulsivity measures. Whole amygdala volumes were not associated with aggression or impulsivity, but significant correlations were found when dorsal/ventral amygdalae were analyzed separately. Specifically, left and right ventral amygdala volume was positively associated with motor impulsivity, and left dorsal amygdala was negatively associated with aggression. Results are discussed in terms of an activation and control model of brain-behavior relations. Potential relevance to the continuum of amygdala hyper- to hypo-activation and aggression is discussed.

In recent years, a common approach to understanding how the basal ganglia contribute to learning and memory in humans has been to study the deficits that occur in patients with basal ganglia pathology, such as Parkinson's disease and Huntington's disease. Pharmacological manipulations in patients and in healthy volunteers have also been conducted to investigate the role of dopamine, a neurotransmitter that is crucial for normal striatal functioning. When combined with powerful functional neuroimaging methods such as positron emission tomography and functional magnetic resonance imaging, such studies can provide important new insights into striatal function and dysfunction in humans. In this review, we consider this broad literature in an attempt to define a specific role for the caudate nucleus in learning and memory, and in particular, how this role may differ from that of the putamen. We conclude that the caudate nucleus contributes to learning and memory through the excitation of correct action schemas and the selection of appropriate sub-goals based on an evaluation of action-outcomes; both processes that are fundamental to all tasks involve goal-directed action.

Abstract BACKGROUND: Positron emission tomography (PET) studies of major depression have revealed resting-state abnormalities in the prefrontal and cingulate cortices. Recently, fMRI has been adapted to examine connectivity within a specific resting-state neural network--the default-mode network--that includes medial prefrontal and anterior cingulate cortices. The goal of this study was to examine resting-state, default-mode network functional connectivity in subjects with major depression and in healthy controls. METHODS: Twenty-eight subjects with major depression and 20 healthy controls underwent 5-min fMRI scans while resting quietly. Independent component analysis was used to isolate the default-mode network in each subject. Group maps of the default-mode network were compared. A within-group analysis was performed in the depressed group to explore effects of depression refractoriness on functional connectivity. RESULTS: Resting-state subgenual cingulate and thalamic functional connectivity with the default-mode network were significantly greater in the depressed subjects. Within the depressed group, the length of the current depressive episode correlated positively with functional connectivity in the subgenual cingulate. CONCLUSIONS: This is the first study to explore default-mode functional connectivity in major depression. The findings provide cross-modality confirmation of PET studies demonstrating increased thalamic and subgenual cingulate activity in major depression. Further, the within-subject connectivity analysis employed here brings these previously isolated regions of hypermetabolism into the context of a disordered neural network. The correlation between refractoriness and subgenual cingulate functional connectivity within the network suggests that a quantitative, resting-state fMRI measure could be used to guide therapy in individual subjects.

Major Depressive Disorder (MDD) has been conceptualized as a neural network-level disease. Few studies of the neural bases of depression, however, have used analytic techniques that are capable of testing network-level hypotheses of neural dysfunction in this disorder. Moreover, of those that have, fewer still have attempted to determine directionality of influence within functionally abnormal networks of structures. We used multivariate Granger causality analysis a technique that estimates the extent to which preceding neural activity in one or more seed regions predicts subsequent activity in target brain regions to analyze blood-oxygen-level dependent (BOLD) data collected during eyes-closed rest in depressed and never-depressed persons. We found that activation in the hippocampus predicted subsequent increases in ventral anterior cingulate cortex (vACC) activity in depression, and that activity in medial prefrontal cortex and vACC were mutually reinforcing in MDD. Hippocampal and vACC activation in depressed participants predicted subsequent decreases in dorsal cortical activity. This study shows that, on a moment-by-moment basis, there is increased excitatory activity among limbic and paralimbic structures, as well as increased inhibition in activity of dorsal cortical structures, by limbic structures in depression; these aberrant patterns of effective connectivity implicate disturbances in the mesostriatal dopamine system in depression. These findings advance neural theory of depression by detailing specific patterns of limbic excitation in MDD, by making explicit the primary role of limbic inhibition of dorsal cortex in the cortico-limbic relation posited to underlie depression, and by presenting an integrated neurofunctional account of altered dopamine function in this disorder.

AbstractBackgroundAggression in borderline personality disorder (BPD) is thought to be mediated through emotion dysregulation via high trait anger. Until now, data comparing anger and aggression in female and male patients with BPD have been widely missing on the behavioral and particularly the brain levels.MethodsThirty-three female and 23 male patients with BPD and 30 healthy women and 26 healthy men participated in this functional magnetic resonance imaging study. We used a script-driven imagery task consisting of narratives of both interpersonal rejection and directing physical aggression toward others.ResultsWhile imagining both interpersonal rejection and acting out aggressively, a sex × group interaction was found in which male BPD patients revealed higher activity in the left amygdala than female patients. In the aggression phase, men with BPD exhibited higher activity in the lateral orbitofrontal and dorsolateral prefrontal cortices compared with healthy men and female patients. Positive connectivity between amygdala and posterior middle cingulate cortex was found in female patients but negative connectivity was found in male patients with BPD. Negative modulatory effects of trait anger on amygdala–dorsolateral prefrontal cortex and amygdala–lateral orbitofrontal cortex coupling were shown in male BPD patients, while in female patients trait anger positively modulated dorsolateral prefrontal cortex–amygdala coupling. Trait aggression was found to positively modulate connectivity of the left amygdala to the posterior thalamus in male but not female patients.ConclusionsData suggest poor top-down adjustment of behavior in male patients with BPD despite their efforts at control. Female patients appear to be less aroused through rejection and to successfully dampen aggressive tension during the imagination of aggressive behavior.

A significant proportion of patients with schizophrenia demonstrate abnormalities in dorsal prefrontal regions including the dorsolateral prefrontal and dorsal anterior cingulate cortices. However, it is less clear to what extent abnormalities are exhibited in ventral prefrontal and limbic regions, despite their involvement in social cognitive dysfunction and aggression, which represent problem domains for patients with schizophrenia. Previously, we found that reduced white matter integrity in right inferior frontal regions was associated with higher levels of aggression. Here, we used resting-state functional magnetic resonance imaging to examine amygdala/ventral prefrontal cortex (vPFC) functional connectivity (FC) and its relation to aggression in schizophrenia. Twenty-one healthy controls and 25 patients with schizophrenia or schizoaffective disorder participated. Aggression was measured using the Buss Perry Aggression Questionnaire. Regions of interest were placed in the amygdala based on previously published work. A voxelwise FC analysis was performed in which the mean time series across voxels for this bilateral amygdala seed was entered as a predictor in a multiple regression model with motion parameters and global, cerebrospinal fluid, and white matter signals as covariates. Patients showed significant reductions in FC between amygdala and vPFC regions. Moreover, in patients, the strength of this connection showed a significant inverse relationship with aggression, such that lower FC was associated with higher levels of self-rated aggression. Similar results were obtained for 2 other measures--Life History of Aggression and total arrests. These results suggest that amygdala/vPFC FC is compromised in schizophrenia and that this compromise is associated with aggression.

Abstract Vasopressin and oxytocin strongly modulate autonomic fear responses, through mechanisms that are still unclear. We describe how these neuropeptides excite distinct neuronal populations in the central amygdala, which provides the major output of the amygdaloid complex to the autonomic nervous system. We identified these two neuronal populations as part of an inhibitory network, through which vasopressin and oxytocin modulate the integration of excitatory information from the basolateral amygdala and cerebral cortex in opposite manners. Through this network, the expression and endogenous activation of vasopressin and oxytocin receptors may regulate the autonomic expression of fear.

Aggressive behavior is a basic form of human social interaction, yet little is known about its neural substrates. We used a laboratory task to investigate the neural correlates of reactive aggression using functional magnetic resonance imaging. The task is disguised as a reaction-time competition between the subject and two opponents and entitles the winner to punish the loser. It seeks to elicit aggression by provocation of the subject. As each single trial in this task is separated into a decision phase, during which the severity of the prospective punishment of the opponent is set, and an outcome phase, during which the actual punishment is applied or received, the paradigm enables us to analyze the neural events during each of these phases. Specific neural responses in areas related to negative affect, cognitive control and reward processing provide additional information about the cognitive, emotional and motivational processes underlying reactive aggressive behavior and afford us with the possibility to test and expand theories on aggression such as the General Aggression Model.

Abstract In recent years, there has been an explosion of interest in the neural basis of emotion. Much of this enthusiasm has been triggered by studies of the amygdala and its contribution to fear. This work has shown that the amygdala detects and organizes responses to natural dangers (like predators) and learns about novel threats and the stimuli that predict their occurrence. The latter process has been studied extensively using a procedure called classical fear conditioning. This article surveys the progress that has been made in understanding the neural basis of fear and its implications for anxiety disorders, as well as the gaps in our knowledge.

The amygdala is thought to be an important neural structure underlying the "fight-or-flight" response, but information on its role in is scarce. The clinical and psychophysiological effects of amygdalar destruction were studied in 2 patients who underwent bilateral amygdalotomy for intractable . After surgery, both patients showed a reduction in autonomic arousal levels to stressful stimuli and in the number of , although both patients continued to have difficulty controlling . The "taming effect" reported after bilateral amygdalar destruction may be due to the amygdala's inadequate processing of perceived threat stimuli that would normally produce a fight-or-flight response.

Previous research has shown that exposure to violent video games increases aggression, whereas exposure to prosocial video games can reduce aggressive behavior. However, little is known about the neural correlates of these behavioral effects. This work is the first to investigate the electrophysiological features of the relationship between playing a prosocial video game and inhibition of aggressive behavior. Forty-nine subjects played either a prosocial or a neutral video game for 20 min, then participated in an event-related potential (ERP) experiment based on an oddball paradigm and designed to test electrophysiological responses to prosocial and violent words. Finally, subjects completed a competitive reaction time task (CRTT) which based on Taylor's Aggression Paradigm and contains reaction time and noise intensity chosen as a measure of aggressive behavior. The results show that the prosocial video game group (compared to the neutral video game group) displayed smaller P300 amplitudes, were more accurate in distinguishing violent words, and were less aggressive as evaluated by the CRTT of noise intensity chosen. A mediation analysis shows that the P300 amplitude evoked by violent words partially mediates the relationship between type of video game and subsequent aggressive behavior. The results support theories based on the General Learning Model. We provide converging behavioral and neural evidence that exposure to prosocial media may reduce aggression.

Interactive paradigms inducing reactive aggression are absent in the brain mapping literature. We used a competitive reaction time task to investigate brain regions involved in social interaction and reactive aggression in sixteen healthy male subjects with fMRI. Subjects were provoked by increasingly aversive stimuli and were given the opportunity to respond aggressively against their opponent by administering a stimulus as retaliation. fMRI revealed an increase of medial prefrontal cortex (mPFC) activity during retaliation. The dorsal mPFC was active when subjects had to select the intensity of the retaliation stimulus, and its activity correlated with the selected stimulus strength. In contrast, ventral mPFC was active during observing the opponent suffering but also during retaliation independent of the stimulus strength. Ventral mPFC activation, stronger in low callous subjects, correlated positively with skin conductance response during observation of the suffering opponent. In conclusion, dorsal mPFC activation seems to represent cognitive operations related to more intense social interaction processes whereas the ventral mPFC might be involved in affective processes associated with compassion to the suffering opponent.

Learning the relationships between aversive events and the environmental stimuli that predict such events is essential to the survival of organisms throughout the animal kingdom. Pavlovian fear conditioning is an exemplar of this form of learning that is exhibited by both rats and humans. Recent years have seen an incredible surge in interest in the neurobiology of fear conditioning. Neural circuits underlying fear conditioning have been mapped, synaptic plasticity in these circuits has been identified, and biochemical and genetic manipulations are beginning to unravel the molecular machinery responsible for the storage of fear memories. These advances represent an important step in understanding the neural substrates of a rapidly acquired and adaptive form of associative learning and memory in mammals.

Abstract BACKGROUND: Individuals with intermittent explosive disorder (IED) were previously found to exhibit amygdala hyperactivation and relatively reduced orbital medial prefrontal cortex (OMPFC) activation to angry faces while performing an implicit emotion information processing task during functional magnetic resonance imaging (fMRI). This study examines the neural substrates associated with explicit encoding of facial emotions among individuals with IED. METHOD: Twenty unmedicated IED subjects and twenty healthy, matched comparison subjects (HC) underwent fMRI while viewing blocks of angry, happy, and neutral faces and identifying the emotional valence of each face (positive, negative or neutral). We compared amygdala and OMPFC reactivity to faces between IED and HC subjects. We also examined the relationship between amygdala/OMPFC activation and aggression severity. RESULTS: Compared to controls, the IED group exhibited greater amygdala response to angry (vs. neutral) facial expressions. In contrast, IED and control groups did not differ in OMPFC activation to angry faces. Across subjects amygdala activation to angry faces was correlated with number of prior aggressive acts. CONCLUSIONS: These findings extend previous evidence of amygdala dysfunction in response to the identification of an ecologically-valid social threat signal (processing angry faces) among individuals with IED, further substantiating a link between amygdala hyperactivity to social signals of direct threat and aggression. Copyright 漏 2016. Published by Elsevier Ltd.

Why are children of poor parents more likely to be poor as adults than other children? Early-childhood adversities resulting from social structures and relation

Abstract Linking psychopathy to a specific brain abnormality could have significant clinical, legal, and scientific implications. Theories on the neurobiological basis of the disorder typically propose dysfunction in a circuit involving ventromedial prefrontal cortex (vmPFC). However, to date there is limited brain imaging data to directly test whether psychopathy may indeed be associated with any structural or functional abnormality within this brain area. In this study, we employ two complementary imaging techniques to assess the structural and functional connectivity of vmPFC in psychopathic and non-psychopathic criminals. Using diffusion tensor imaging, we show that psychopathy is associated with reduced structural integrity in the right uncinate fasciculus, the primary white matter connection between vmPFC and anterior temporal lobe. Using functional magnetic resonance imaging, we show that psychopathy is associated with reduced functional connectivity between vmPFC and amygdala as well as between vmPFC and medial parietal cortex. Together, these data converge to implicate diminished vmPFC connectivity as a characteristic neurobiological feature of psychopathy.

Abstract The purpose of this communication is to present the results of stereotaxic oil-wax destruction of the amygdaloid nucleus, either unilaterally or bilaterally, on behavior disturbances. It was originally our intention to investigate the value of amygdalotomy upon patients with temporal lobe epilepsy characterized by psychomotor seizures and focal spike discharges on the electroencephalogram as well as marked behavior disturbances such as hyperexcitability, assaultive behavior, or violent aggressiveness. The indications for amygdalotomy were then extended to include patients without clinical manifestations of temporal lobe epilepsy but with EEG abnormalities and marked behavior disturbances. Finally, cases of behavior disorders without epileptic manifestations, clinically and electrically, but associated with various degrees of feeblemindedness or with subnormal intelligence were also included in the series. It has been known for a long time that patients with temporal lobe seizures often exhibit disturbances of emotional behavior and conversely, that patients manifesting abnormalities of general behavior frequently

The purpose of the present study was: first, to offer a few theoretical considerations on the concept of human aggression and its main types; and second, to analyse the relationship between those types of aggression and other related psychological constructs, such as anger, hostility, and impulsivity, summarizing the main empirical results of our research in progress. In order to assess their eventual correlations, several self-report techniques were compared: (a) AQ, used to measure several kinds of aggression, anger, and hostility; (b) CAMA, a questionnaire already used in a variety of cultures, for measuring attitudes toward interpersonal aggression in different instrumental and hostile situations; (c) ASQ, an instrument for measuring experienced anger and its expression in assertive or aggressive ways; and (d) BIS, used to prove three impulsiveness sub-traits: motor, attentional, and non-planning impulsiveness. The different definitions of aggression may be grouped according to whether the primary goal is distress or harm, focusing primarily on the objective infliction of harm, or on the subjective intention of harming. Most classifications in the literature show two kinds of aggression, even if different names are used: Hostile Aggression (among other names it is also known as ‘reactive, impulsive, or affective’) is an act primarily oriented to hurt another individual; and Instrumental Aggression (also known as ‘proactive, premeditated, or predative’) is a means or tool for solving problems or for obtaining a variety of objectives. As predicted, there was a positive correlation between experience and expression of anger. Anger involved physiological arousal and prepared for aggression. Anger and impulsiveness were also positively correlated with hostile aggression, but not with instrumental aggression. In the case of impulsiveness, non-planning impulsiveness was positively correlated with some situations related to hostile aggression, such as emotional agitation or lack of communication, but not with instrumental one. Finally, hostility positively correlated with anger and different kinds of aggression, but not its degree of justification. In sum, aggression can be reflected in the different personality constructs, measured by self-reports.

Aggression and violence represent a significant public health concern and a clinical challenge for the mental healthcare provider. A great deal has been revealed regarding the neurobiology of violence and aggression, and an integration of this body of knowledge will ultimately serve to advance clinical diagnostics and therapeutic interventions. We will review here the latest findings regarding the neurobiology of aggression and violence. First, we will introduce the construct of aggression, with a focus on issues related to its heterogeneity, as well as the importance of refining the aggression phenotype in order to reduce pathophysiologic variability. Next we will examine the neuroanatomy of aggression and violence, focusing on regional volumes, functional studies, and interregional connectivity. Significant emphasis will be on the amygdala, as well as amygdala-frontal circuitry. Then we will turn our attention to the neurochemistry and molecular genetics of aggression and violence, examining the extensive findings on the serotonergic system, as well as the growing literature on the dopaminergic and vasopressinergic systems. We will also address the contribution of steroid hormones, namely, cortisol and testosterone. Finally, we will summarize these findings with a focus on reconciling inconsistencies and potential clinical implications; and, then we will suggest areas of focus for future directions in the field.

Damage to the ventromedial frontal cortex (VMFC) in humans is associated with deficits in decision making. Decision making, however, often happens while people are interacting with others, where it is important to take the social consequences of a course of action into account. It is well known that VMFC lesions also lead to marked alterations in patients emotions and ability to interact socially; however, it has not been clear which parts of the VMFC are critical for these changes. Recently, there has been considerable interest in the role of the VMFC in choice behavior during interpersonal exchanges. Here, we highlight recent research that suggests that two areas within or adjacent to the VMFC, the orbitofrontal cortex (OFC) and the anterior cingulate cortex (ACC), may play distinct but complementary roles in mediating normal patterns of emotion and social behavior. Converging lines of evidence from human, macaque, and rat studies now suggest that the OFC may be more specialized for simple emotional responses, such as fear and aggression, through its role in representing primary reinforcement or punishment. By contrast, the ACC may play a distinct role in more complex aspects of emotion, such as social interaction, by virtue of its connections with the discrete parts of the temporal lobe and subcortical structures that control autonomic responses.

Attention-deficit/hyperactivity disorder (ADHD) is currently defined as a cognitive/behavioral developmental disorder where all clinical criteria are behavioral. Inattentiveness, overactivity, and impulsiveness are presently regarded as the main clinical symptoms. The dynamic developmental behavioral theory is based on the hypothesis that altered dopaminergic function plays a pivotal role by failing to modulate nondopaminergic (primarily glutamate and GABA) signal transmission appropriately. A hypofunctioning mesolimbic dopamine branch produces altered reinforcement of behavior and deficient extinction of previously reinforced behavior. This gives rise to delay aversion, development of hyperactivity in novel situations, impulsiveness, deficient sustained attention, increased behavioral variability, and failure to "inhibit" responses ("disinhibition"). A hypofunctioning mesocortical dopamine branch will cause attention response deficiencies (deficient orienting responses, impaired saccadic eye movements, and poorer attention responses toward a target) and poor behavioral planning (poor executive functions). A hypofunctioning nigrostriatal dopamine branch will cause impaired modulation of motor functions and deficient nondeclarative habit learning and memory. These impairments will give rise to apparent developmental delay, clumsiness, neurological "soft signs," and a "failure to inhibit" responses when quick reactions are required. Hypofunctioning dopamine branches represent the main individual predispositions in the present theory. The theory predicts that behavior and symptoms in ADHD result from the interplay between individual predispositions and the surroundings. The exact ADHD symptoms at a particular time in life will vary and be influenced by factors having positive or negative effects on symptom development. Altered or deficient learning and motor functions will produce special needs for optimal parenting and societal styles. Medication will to some degree normalize the underlying dopamine dysfunction and reduce the special needs of these children. The theory describes how individual predispositions interact with these conditions to produce behavioral, emotional, and cognitive effects that can turn into relatively stable behavioral patterns.

Abstract A converging body of literature over the last 50 years has implicated the amygdala in assigning emotional significance or value to sensory information. In particular, the amygdala has been shown to be an essential component of the circuitry underlying fear-related responses. Disorders in the processing of fear-related information are likely to be the underlying cause of some anxiety disorders in humans such as posttraumatic stress. The amygdaloid complex is a group of more than 10 nuclei that are located in the midtemporal lobe. These nuclei can be distinguished both on cytoarchitectonic and connectional grounds. Anatomical tract tracing studies have shown that these nuclei have extensive intranuclear and internuclear connections. The afferent and efferent connections of the amygdala have also been mapped in detail, showing that the amygdaloid complex has extensive connections with cortical and subcortical regions. Analysis of fear conditioning in rats has suggested that long-term synaptic plasticity of inputs to the amygdala underlies the acquisition and perhaps storage of the fear memory. In agreement with this proposal, synaptic plasticity has been demonstrated at synapses in the amygdala in both in vitro and in vivo studies. In this review, we examine the anatomical and physiological substrates proposed to underlie amygdala function.

Studies addressing the neural correlates of criminal behavior have focused primarily on the prefrontal cortex and the amygdala. However, few studies have examined dopaminergic inputs to these or other brain regions, despite the fact that central dopamine (DA) dysfunction is associated with both trait impulsivity and novelty seeking. Given long-standing associations between both of these personality traits and externalizing psychopathology, the authors examined effective connectivity between the caudate nucleus and the anterior cingulate cortex, two areas that rely on DA input to facilitate associative learning and goal directed behavior. Dysfunction in top-down and bottom-up processing within this dopaminergically mediated frontostriatal circuit may be an important biological vulnerability that increases one likelihood of engaging in delinquent and criminal behavior. When compared with controls, reduced effective connectivity between these regions among adolescents with externalizing psychopathology was found, suggesting deficiencies in frontostriatal circuitry.

Aggression and violence represent a significant public health concern and a clinical challenge for the mental healthcare provider. A great deal has been revealed regarding the neurobiology of violence and aggression, and an integration of this body of knowledge will ultimately serve to advance clinical diagnostics and therapeutic interventions. We will review here the latest findings regarding the neurobiology of aggression and violence. First, we will introduce the construct of aggression, with a focus on issues related to its heterogeneity, as well as the importance of refining the aggression phenotype in order to reduce pathophysiologic variability. Next we will examine the neuroanatomy of aggression and violence, focusing on regional volumes, functional studies, and interregional connectivity. Significant emphasis will be on the amygdala, as well as amygdala芒聙聯frontal circuitry. Then we will turn our attention to the neurochemistry and molecular genetics of aggression and violence, examining the extensive findings on the serotonergic system, as well as the growing literature on the dopaminergic and vasopressinergic systems. We will also address the contribution of steroid hormones, namely, cortisol and testosterone. Finally, we will summarize these findings with a focus on reconciling inconsistencies and potential clinical implications; and, then we will suggest areas of focus for future directions in the field.

Resting-state fMRI (RS-fMRI) has been drawing more and more attention in recent years. However, a publicly available, systematically integrated and easy-to-use tool for RS-fMRI data processing is still lacking. We developed a toolkit for the analysis of RS-fMRI data, namely the RESting-state fMRI data analysis Toolkit (REST). REST was developed in MATLAB with graphical user interface (GUI). After data preprocessing with SPM or AFNI, a few analytic methods can be performed in REST, including functional connectivity analysis based on linear correlation, regional homogeneity, amplitude of low frequency fluctuation (ALFF), and fractional ALFF. A few additional functions were implemented in REST, including a DICOM sorter, linear trend removal, bandpass filtering, time course extraction, regression of covariates, image calculator, statistical analysis, and slice viewer (for result visualization, multiple comparison correction, etc.). REST is an open-source package and is freely available at http://www.restfmri.net.

The analysis of functional connectivity at rest (rFC) enables us to know how brain regions within and between networks interact. In this study, we used resting-state functional magnetic resonance imaging and a creativity test of divergent thinking (DT) to investigate the relationship between creativity measured by DT and rFC. We took the medial prefrontal cortex (mPFC) to be the seed region and investigated correlations across subjects between the score of the DT test and the strength of rFC between the mPFC and other brain regions. Our results showed that the strength of rFC with the mPFC significantly and positively correlated with creativity as measured by the DT test in the posterior cingulate cortex (PCC). These results showed that higher creativity measured by DT is associated with rFC between the mPFC and the PCC, the key nodes of the default mode network (DMN). Increased rFC between these regions is completely opposite from that is generally expected from the association between higher creativity and reduced deactivation in DMN during an externally directed attention-demanding task shown in our previous study but is similar to the pattern seen in relatives of schizophrenia. These findings are comparable to the previously reported psychological associations between schizotypy and creativity.

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An anatomical parcellation of the spatially normalized single-subject high-resolution T1 volume provided by the Montreal Neurological Institute (MNI) (D. L. Collins et al., 1998, Trans. Med. Imag. 17, 463鈥468) was performed. The MNI single-subject main sulci were first delineated and further used as landmarks for the 3D definition of 45 anatomical volumes of interest (AVOI) in each hemisphere. This procedure was performed using a dedicated software which allowed a 3D following of the sulci course on the edited brain. Regions of interest were then drawn manually with the same software every 2 mm on the axial slices of the high-resolution MNI single subject. The 90 AVOI were reconstructed and assigned a label. Using this parcellation method, three procedures to perform the automated anatomical labeling of functional studies are proposed: (1) labeling of an extremum defined by a set of coordinates, (2) percentage of voxels belonging to each of the AVOI intersected by a sphere centered by a set of coordinates, and (3) percentage of voxels belonging to each of the AVOI intersected by an activated cluster. An interface with the Statistical Parametric Mapping package (SPM, J. Ashburner and K. J. Friston, 1999, Hum. Brain Mapp. 7, 254鈥266) is provided as a freeware to researchers of the neuroimaging community. We believe that this tool is an improvement for the macroscopical labeling of activated area compared to labeling assessed using the Talairach atlas brain in which deformations are well known. However, this tool does not alleviate the need for more sophisticated labeling strategies based on anatomical or cytoarchitectonic probabilistic maps.

Abstract Decision making is guided by the likely consequences of behavioural choices. Neuronal correlates of financial reward have been described in a number of functional imaging studies in humans. Areas implicated in reward include ventral striatum, dopaminergic midbrain, amygdala and orbitofrontal cortex. Response to loss has not been as extensively studied but may involve prefrontal and medial temporal cortices. It has been proposed that increased sensitivity to reward and reduced sensitivity to punishment underlie some of the psychopathology in impulsive personality disordered individuals. However, few imaging studies using reinforcement tasks have been conducted in this group. In this fMRI study, we investigate the effects of positive (monetary reward) and negative (monetary loss) outcomes on BOLD responses in two target selection tasks. The experimental group comprised eight people with Cluster B (antisocial and borderline) personality disorder, whilst the control group contained fourteen healthy participants. A key finding was the absence of prefrontal responses and reduced BOLD signal in the subcortical reward system in the PD group during positive reinforcement. Impulsivity scores correlated negatively with prefrontal responses in the PD but not the control group during both, reward and loss. Our results suggest dysfunctional responses to rewarding and aversive stimuli in Cluster B personality disordered individuals but do not support the notion of hypersensitivity to reward and hyposensitivity to loss.

Treatment-refractory depression (TRD) represents a large proportion of the depressive population, yet has seldom been investigated using advanced imaging techniques. To characterize brain dysfunction in TRD, we performed resting-state functional MRI (rs-fMRI) on 22 TRD patients, along with 26 matched healthy subjects and 22 patients who were depressed but not treatment-refractory (NDD) as comparison groups. Results were analyzed using a data-driven approach known as Regional Homogeneity (ReHo) analysis which measures the synchronization of spontaneous fMRI signal oscillations within spatially neighboring voxels. Relative to healthy controls, both depressed groups showed high ReHo primarily within temporo-limbic structures, and more widespread low ReHo in frontal, parietal, posterior fusiform cortices, and caudate. TRD patients showed more cerebral regions with altered ReHo than did NDD. Moderate but significant correlations between the altered regional ReHo and measures of clinical severity were observed in some identified clusters. These findings shed light on the pathophysiological mechanisms underlying TRD and demonstrate the feasibility of using ReHo as a research and clinical tool to monitor persistent cerebral dysfunction in depression, although further work is necessary to compare different measures of brain function to elucidate the neural substrates of these ReHo abnormalities. Hum Brain Mapp, 2011. 2010 Wiley-Liss, Inc.

Resting-state functional magnetic resonance imaging (fMRI) has attracted more and more attention because of its effectiveness, simplicity and non-invasiveness in exploration of the intrinsic functional architecture of the human brain. However, user-friendly toolbox for “pipeline” data analysis of resting-state fMRI is still lacking. Based on some functions in Statistical Parametric Mapping (SPM) and Resting-State fMRI Data Analysis Toolkit (REST), we have developed a MATLAB toolbox called Data Processing Assistant for Resting-State fMRI (DPARSF) for “pipeline” data analysis of resting-state fMRI. After the user arranges the Digital Imaging and Communications in Medicine (DICOM) files and click a few buttons to set parameters, DPARSF will then give all the preprocessed (slice timing, realign, normalize, smooth) data and results for functional connectivity, regional homogeneity, amplitude of low-frequency fluctuation (ALFF), and fractional ALFF. DPARSF can also create a report for excluding subjects with excessive head motion and generate a set of pictures for easily checking the effect of normalization. In addition, users can also use DPARSF to extract time courses from regions of interest.

Recent resting-state functional connectivity magnetic resonance imaging studies have shown significant group differences in several regions and networks between patients with major depressive disorder and healthy controls. The objective of the present study was to investigate the whole-brain resting-state functional connectivity patterns of depressed patients, which can be used to test the feasibility of identifying major depressive individuals from healthy controls. Multivariate pattern analysis was employed to classify 24 depressed patients from 29 demographically matched healthy volunteers. Permutation tests were used to assess classifier performance. The experimental results demonstrate that 94.3% (P鈥<鈥0.0001) of subjects were correctly classified by leave-one-out cross-validation, including 100% identification of all patients. The majority of the most discriminating functional connections were located within or across the default mode network, affective network, visual cortical areas and cerebellum, thereby indicating that the disease-related resting-state network alterations may give rise to a portion of the complex of emotional and cognitive disturbances in major depression. Moreover, the amygdala, anterior cingulate cortex, parahippocampal gyrus and hippocampus, which exhibit high discriminative power in classification, may play important roles in the pathophysiology of this disorder. The current study may shed new light on the pathological mechanism of major depression and suggests that whole-brain resting-state functional connectivity magnetic resonance imaging may provide potential effective biomarkers for its clinical diagnosis.

Although one proposed function of both the striatum and its major dopamine inputs is related to coding rewards and reward-related stimuli, an alternative view suggests a more general role of the striatum in processing salient events, regardless of their reward value. Here we define saliency as an event that both is unexpected and elicits an attentional-behavioral switch (i.e., arousing). In the present study, human striatal responses to nonrewarding salient stimuli were investigated. Using functional magnetic resonance imaging (fMRI), the blood oxygenation level-dependent signal was measured in response to flickering visual distractors presented in the background of an ongoing task. Distractor salience was manipulated by altering the frequency of distractor occurrence. Infrequently presented distractors were considered more salient than frequently presented distractors. We also investigated whether behavioral relevance of the distractors was a necessary component of saliency for eliciting striatal responses. In the first experiment (19 subjects), the distractors were made behaviorally relevant by defining a subset of them as targets requiring a button press. In the second experiment (17 subjects), the distractors were not behaviorally relevant (i.e., they did not require any response). The fMRI results revealed increased activation in the nucleus accumbens after infrequent (high salience) relative to frequent (low salience) presentation of distractors in both experiments. Caudate activity increased only when the distractors were behaviorally relevant. These results demonstrate a role of the striatum in coding nonrewarding salient events. In addition, a functional subdivision of the striatum according to the behavioral relevance of the stimuli is suggested.

Abstract While the striatum has been implicated in reward processing, an alternative view contends that the striatum processes salient events in general. Using fMRI, we investigated human striatal responses to monetary reward while modulating the saliency surrounding its receipt. Money was maximally salient when its receipt depended on a correct response (active) and minimally salient when its receipt was completely independent of the task (passive). The saliency manipulation was confirmed by skin conductance responses and subjective ratings of the stimuli. Significant caudate and nucleus accumbens activations occurred following the active compared to passive money. Such activations were attributed to saliency rather than the motor requirement associated with the active money because striatal activations were not observed when the money was replaced by inconsequential, nonrewarding stimuli. The present study provides evidence that the striatum's role in reward processing is dependent on the saliency associated with reward, rather than value or hedonic feelings.

The human brain is a complex dynamic system capable of generating a multitude of oscillatory waves in support of brain function. Using fMRI, we examined the amplitude of spontaneous low-frequency oscillations (LFO) observed in the human resting brain and the test–retest reliability of relevant amplitude measures. We confirmed prior reports that gray matter exhibits higher LFO amplitude than white matter. Within gray matter, the largest amplitudes appeared along mid-brain structures associated with the “default-mode” network. Additionally, we found that high-amplitude LFO activity in specific brain regions was reliable across time. Furthermore, parcellation-based results revealed significant and highly reliable ranking orders of LFO amplitudes among anatomical parcellation units. Detailed examination of individual low frequency bands showed distinct spatial profiles. Intriguingly, LFO amplitudes in the slow-4 (0.027–0.07302Hz) band, as defined by Buzsáki et al., were most robust in the basal ganglia, as has been found in spontaneous electrophysiological recordings in the awake rat. These results suggest that amplitude measures of LFO can contribute to further between-group characterization of existing and future “resting-state” fMRI datasets.