Skip to main content

Biological Components of Human Aggression

This was my term paper for Biology of the Brain at Empire State College (SUNY) in pursuit of a B.A. in Human Development.


Herein is presented a brief definition and typology of aggression, relevant brain physiology, and the primary sub-cortical neurobiological components of human aggression. It is demonstrated that human aggression is dependent upon three biological systems: the fight – flight system, the behavioral approach system, and the behavioral inhibition system. Explained are the, physiology, function, and aggression mediation of each of these systems.

Definition of Aggression

Aggression has been part of the human condition through out history and continues as a major cause of human conflict to this day. Science has studied aggression in vertebrates for decades, and researchers continue to make new and important findings relative to human aggression. Although there are many different types and causes of aggression, they all have common biological components.

Human aggression is complicated, ranging from mild verbal anger to vicious murder and everything in between. Conflict styles and aggression vary across individuals, sexes, genders, societies, and eras. Aggression is an important part of being human, an aspect of our complicated and diverse selves.

— Agustin Fuentes

The word aggression can describe many different types of acts from shootings and bombings to insults and undeserved criticism (Geen, 2001). Researchers have studied aggression for decades, yet are unable to decide upon a common definition. Johnson says that the complexities of human aggression defy definition (1972, in Renfrew, 1997). Different branches of science define aggression in their own way. One can describe aggression as a behavior, but also as a feeling that can motivate behavior. There are numerous definitions and types of aggression; however, the Oxford Dictionary of Biology provides a definition that conveys a generally accepted meaning of aggression in the field of human behavior: a “behaviour aimed at intimidating or injuring another animal of the same or a competing species" (2000).

However, we do not consider unintentional harm to be aggression (Anderson & Bushman, 2002). There is no scientific consensus on the various types of aggression, but most classifications are similar to or based upon Moyer’s eight types: predatory, inter-male, fear-induced [defense], territorial, maternal, irritable, sex-related, and instrumental (goal oriented) (1976, in Franken, 2002). Numerous factors are involved in the influence and acting out of human aggression, including genetic, environmental, cognitive, neurological, and biological (Geen, 2001; Raine, 2002,).

Brain Physiology and Function

The human brain consists of three primary sections (vesicles) and five secondary vesicles. The forebrain (prosencephalon) consists of the telencephalon (composed primarily of the cerebrum and basal ganglia, which includes the amygdala), and the diencephalon (composed primarily of the thalamus, hypothalamus, pituitary gland, and sensory processing areas). The midbrain consists of the mesencephalon, which is composed of portions of the brain stem. The hindbrain (rhombencephalon) consists of the metencephalon (composed primarily of the pons portion of the brain stem and the cerebellum), and the myelencephalon (composed primarily of the medulla oblongata portion of the brain stem) (Pack, 2001).

Neurobiological components are multi-functional and not limited to activity in only one functional system. The limbic system, coined by MacLean in 1952, provides such an example. The limbic system controls basic emotions, and although scientists do not agree upon its components (Buckley, 2001), it is believed to consist of the amygdala, cingulate gyrus, fornix, hippocampus, mammillary bodies (in the hypothalamus) (Colman, 2001b), parahippocampal gyrus, septum pellucidum, and thalamus (Colman, 2001a).

Function of Neurotransmitters in the Brain

Neurotransmitters are an important part of the central nervous system and enable nerve impulses to bridge the synaptic cleft (Postlethwait & Hopson, 2003).

Some neurotransmitters are important in regulating mood. Researchers have found that serotonin, dopamine, gamma—aminobutyric acid (GABA), norepinephrine, and epinephrine are relevant to human aggression (Renfrew, 1997). In addition to mood regulation, serotonin is also involved in several other physiological processes, such as muscle contraction, the regulation of appetite and perception, and blood platelet grouping. To accommodate these many functions, there are at least fifteen different serotonin receptors (Kroeze, Kristiansen & Roth, 2002).

The reticular activating system (RAS) is part of the reticular formation, a neural network in the brain stem responsible for arousing the cerebral cortex (Colman, 2001c; Tyson, 1988). To conserve energy, the information processing centers of the brain shut down when not needed. The RAS only activates the portions of the brain needed to process current sensory perceptions (Franken, 2002). Although not known for sure, scientists believe that thalamic relay neurons constitute a significant portion of the RAS. These neurons can remain in a state of depolarization, but when the RAS receives new sensory information, the neurons polarize and send the information to the cortex (Reiner, 1995). The thalamus directly connects to both the neocortex and the amygdala. Input from the sensory organs first goes to the thalamus, which acts as a switching station and controls information exchange between the neocortex and basal ganglia [which the amygdala is a part of (“amygdala n.,” 2002)] (Postlethwait and Hopson, 2003; Williams, 1990, in Panksepp, 1998).

Neurobiological Mediation of Aggression

As multi faceted as aggression is, without the biological components, aggression would not occur. Gray has said, “In the long run, any account of behaviour which does not agree with the knowledge of the neuro-endocrine systems…must be wrong” (1972, in Corr, 2004, p. 318).

Function, rather than physiology, defines some neurobiological systems in the brain, and in some cases, science better understands function than the specific physiology that is responsible. In 1964, Jeffrey Gray developed a neuropsychological personality theory known as the reinforcement sensitivity theory (RST) (in Corr, 2004). This theory explains three neurobiological systems that mediate human aggression: the fight – flight system (FFS), the behavioral activation system (BAS), and the behavioral inhibition system (BIS) (Gray, 1991; in Franken, 2002). Many researchers have either modified or built entirely new theories from Gray’s RST. In 2000, Gray and McNaughton revised the RST and changed the FFS to the fight – flight – freeze system (FFFS) and made additional clarifications about the types of behavior each system governs (Corr, 2004). [Note: terms FFS and FFFS are used interchangeably based upon the use by the particular source that is referenced; however, both terms refer to the same system].

Researchers continue to make new proposals involving the RST up to the present day. Therefore, study of the neurobiology of human behavior results in varied and often contradictory findings. However, despite modification of personality theories and re-arranging and re-naming of functional systems, the neurobiological components of human behavior remain the same. Although the names of the functional systems of Gray’s RST are used, concentration is placed upon the neurobiological components that mediate aggression. Researchers may change their beliefs about the triggers and responses of the RST systems; however, the neurobiological components themselves will continue to function the same.

The Fight – Flight System (FFS)

The FFS is associated with the fear emotion. It is responsible for governing avoidance or escape behavior toward aversive stimuli (Franken, 2002; Corr, 2004). This is the same system that makes us jump and our heart start to race when we have been startled. When we experience a real or perceived threat, including pain (Franken, 2002) or punishment (Corr, 2004), the sympathetic nervous system (SNS) activates the body’s fight or flight response (Franken, 2002). LeDoux suggests that humans tend to treat novel stimulus as potentially threatening, which can also lead to FFS activation (1986,1992,1993,1996, in Franken, 2002).

The FFS is comprised of the brain stem, midbrain, amygdala, and hypothalamus as well as many sub-systems and responses (Figure 1) (Sergeant, Van De Poll, & Van Goozen, 1994; Franken, 2002).

Scroll to Continue

The amygdala receives sensory information a few milliseconds before the neocortex. This allows us to react before we are fully conscious of the threat (LeDoux, in Franken, 2002). Pontius has identified the amygdalar visual pathway. This pathway extends directly from the retina, through the thalamus, and to the amygdala and motor system, bypassing the parieto–occipital cortex and cognitive evaluation (2002; in Pontius 2004). Both the amygdala and the neocortex can activate the FFS. The amygdala can also deactivate sub-cortical responses (Blair, 2004). When the FFS activates, the hypothalamus causes the adrenal medulla to start pumping epinephrine into the blood stream to get the body into its highest state of readiness (Purves, Orians, Heller, and Sadava, 2004). Epinephrine causes the heart to speed up, raises blood sugar levels, and causes blood flow to be re-directed from the digestive system to the muscular system (Postlethwait and Hopson, 2003). These changes prepare the body to either stay and fight the perceived threat (aggression), or flee.

If the FFS remains activated, the hypothalamus causes the release of corticotrophin-releasing hormone (CRH) into the bloodstream. CRH binds to the anterior pituitary, causing the release of adrenocorticotropic hormone (ACTH) into the bloodstream. ACTH then stimulates the adrenal cortex to produce cortisol, which causes the liver to make immediate energy available by changing proteins and lipids into glucose. When the threat is gone and the body no longer needs to maintain maximum readiness, the FFS deactivates. This occurs when cortisol circulating in the blood stream triggers the hypothalamus and pituitary to cease production of CRH and ACTH (Postlethwait and Hopson, 2003).

Several researchers have linked the FFS to aggression (Lorimer, 1972, in Renfrew, 1997; Zillmann, 1979; Tyson, 1998). The amygdala is able to generate fear responses (Blair et al, 1999, Hornak et al, 1996, Young et al, 1996, in Critchley, Simmons, Daly, Russell, van Amelsvoort, Robertson, et al, 2000), and is linked to the expression and regulation of aggression (Renfrew, 1997; Bear, 1991, Fuster, 1989, in Cairns & Stoff, 1996; Zillmann, 1979). The hypothalamus has also been linked to aggression (George, Rawlings, Williams, Phillips, Fong, Kerich, Momenan, Umhau, & Hommer, 2004; Veenema, Meijer, de Kloet, Koolhaas, & Bohus, 2003;Yao, Rameshwar, Donnelly, & Siegel, 1999). Ramamurthi found that bilateral amygdalectomies reduced aggressive behavior in 70-76% of cases (1988, in Blair, 2004). Animal research reveals that stimulation of the amygdala results in aggression (Siegel & Brutus, 1990, and Shaikh, Schubert, and Siegel, 1994, in Siegel & Shaikh, 1997) and lesions to or removal of the amygdala leads to passivity or reduced aggression (McGregor and Herbert, 1992; in Critchley, Simmons, Daly, Russell, van Amelsvoort, Robertson, et al, 2000). Research indicates that in both animals and humans, the frontal cortex is able to mediate sub-cortical aggression (Anderson, Bechara, Damasio, Tranel, & Damasio, 1999; Grafman, Schwab, Warden, Pridgen, & Brown, 1996; Gregg & Siegel, 2001; Panksepp, 1998; Pennington & Bennetto, 1993, in Blair, 2004).

Under normal circumstances, non-instrumental human aggression requires a normally operating FFS and a perceived threat to activate it. Dozier cites a famous case involving Charles Whitman. Mr. Whitman had no history of violence, but without warning, killed his wife and mother, and then the next day began randomly shooting people with a high-powered rifle a top the tower of the administration building at the University of Texas. He killed fourteen people and wounded twenty-four. An autopsy showed evidence that a tumor was pressing against his amygdala (1998, in Franken, 2002).

The Behavioral Approach System (BAS)

The BAS has several different names: the behavioral approach system (Gray, 1972, 1994a, in Carver, 2004), the behavioral activation system (Fowles, 1980, 1987, in Carver, 2004), the behavioral facilitation system (Depue & Collins, 1999; in Carver, 2004), the reward pathway, and the dopamine pathway (Franken, 2002). There are actually four dopamine pathways: the mesolimbic, mesocortical, nigrostriatal, and tuberoinfundibular (University of Colorado Health Sciences Center, 1999). The dopamine pathways are the primary components that make up the BAS. The mesolimbic pathway is the pathway most connected to dopamine and reward. It extends from the ventral tegmental area (VTA) of the brain through the nucleus accumbens to the prefrontal cortex (Figure 2) (Franken, 2002).

Dopamine, a monoamine, is just one of the many neurotransmitters used by the brain. Each neurotransmitter can have several different kinds of receptors. Such variability of neurotransmitters and receptors allows the brain to perform such varied and complex functions (Kalat, 1995, in Franken, 2002). Dopamine has five receptors, labeled D1 – D5 (Civelli, Bunzow, & Grandy, 1993, in Guy, Hogan, & Keltner, 2001). A chain of metabolic processes creates dopamine. The amino acids phenylalanine and tyrosine create levodopa, the precursor to dopamine.

When dopamine beta hydroxylase metabolizes dopamine, it creates norepinephrine (Guy, Hogan, Keltner, 2001). Low levels of dopamine are associated with Parkinson’s disease and abnormally high levels of dopamine are connected to schizophrenia (Beebe, 2003; Bailey, 1987).

The BAS is an appetitive motivation system (Carver, 2004) that, according to Gray, produces a positive feeling when activated (1981, 1990, 1994b, in Carver, 2004). The BAS governs behavioral response to appetitive stimuli (Corr, 2004) and is responsible for producing feelings of reward for instrumental behaviors that surmount obstacles or avoid punishment (Franken, 2002). Stimulus associated with either reward or punishment avoidance activates the BAS, which acts as a positive feedback loop by motivating the individual to increase proximity to the stimuli, which in turn further activates the BAS and elicits feelings of reward (Sergeant, Van De Poll, & Van Goozen, 1994).

Under normal conditions, the BAS releases dopamine to reinforce or “reward” instrumental behavior essential for survival (Sergeant, Van De Poll, & Van Goozen, 1994). This system is also responsible for Buck's selfish affect system, which triggers motivation for self-preservation, and his prosocial affect system, which triggers motivation for species preservation (1999, in Franken, 2002). The BAS provides the pleasure drive for many essential human activities, such as eating and reproduction -- these are natural rewards. This system also makes unnatural rewards, such as alcohol and certain narcotics, pleasurable and addictive by keeping the dopamine pathway active for an extended period (Comings & Blum, 2000; Sergeant, Van De Poll, & Van Goozen, 1994).

However, frustration resulting from the obstruction of goal attainment often results in anger and can lead to aggression (Dollard, Doob, Miller, Mowrer, & Sears, 1939, and Berkowitz, 1989, 1993a, in Berkowitz & Harmon-Jones, 2004). Affective aggression is positively correlated with anger and hostile attitude, especially if resulting from aversive stimulus (Berkowitz & Harmon-Jones, 2004) or an independent agent deemed responsible for aversive stimulus (Ellsworth & Smith, 1988, Scherer, 2001a, Smith & Ellsworth, 1985, Lazarus, 1991, in Berkowitz & Harmon-Jones, 2004). Additionally, if an individual has experienced reward (resulting in increased dopamine levels) as a result of aggression, the BAS will continue to reward such aggressive behavior. Artificially increased dopamine levels in research animals have demonstrated increased aggression levels (Cairns & Stoff, 1996; Höglund, Korzan, Watt, Forster, Summers, Johannessen, Renner, & Summers, 2004; Rodriguiz, Chu, Caron, & Wetsel, 2004, & Bondar & Kudriavtseva, 2003).

The Behavioral Inhibition System (BIS)

The behavioral inhibition system (Gray, 1972, 1994a, in Franken, 2002) is also known as the withdrawal system (Davidson, 1992, 1998, in Carver, 2004). The biological components of the BIS include the septo-hippocampus system, monoamine afferents (neurotransmitters), frontal cortex (Gray, 1982, in Franken, 2002), and amygdala (McNaughton & Corr, 2004). Conflict between the FFFS and BAS (approach – avoidance) or within (approach – approach or avoidance – avoidance) activates the BIS, but only if both sides of the conflict are fairly balanced (McNaughton & Corr, 2004). When activated, the BIS works to resolve goal conflict by performing increased risk assessment, approach and avoidance behavior inhibition (not immobility), incrementally increased arousal and attention, and exploratory behavior, all of which is emotionally experienced as anxiety (Corr, 2004; Sergeant & Van De Pool, & Goozen, 1994; Franken, 2002; McNaughton & Corr, 2004).


This is the “stop look and listen system” (Gray, 1991, in Franken, 2002), which acts as a braking system for the BAS. Novel stimuli as well as stimuli that produces punishment or reward cessation activates the BIS. Research indicates that organisms need full knowledge about their surroundings to survive. An example is the rabbit's practice of exploring all escape routes to be prepared for an enemy encounter. Environmental change poses a possible threat, which causes the rabbit to investigate. In such an instance, Gray says that the rabbit stops, looks, and listens when encountering novel stimuli (in Franken, 2002).

Anxiety is the emotion associated with the BIS (Sergeant, Van De Poll, & Van Goozen, 1994). Gray says that the BIS mediates anxiety, which is proven by the fact that anti-anxiety pharmocologics do not affect the FFS - only the BIS. Anti-anxiety drugs work by deactivating the BIS (in Franken, 2002). Some of these drugs inhibit the reuptake of serotonin, which increases the level of serotonin in synapses. Increased serotonin levels in animals has resulted in lower aggression levels (Larson, 2001, in Summers, Summers, Moore, Korzan, Woodley, et al 2003) and decreased serotonin levels in humans and other animals are correlated with aggression (Miczek, Fish, de Bold, & de Almeida, 2002; Field, 2002; Lesch & Merschdorf, 2000). Low serotonin levels increase the potential for aggression and impulsiveness (Buck, 1999, in Franken, 2002; Panksepp, 1988; Linnoila, Virkkunen, Scheinin, Nuutila, Rimon, and Goodwin, 1983).

Impulsivity is a correlating factor of aggression (Barratt, 1994, Hart & Dempster, 1997, McMurran, Blair, & Egan, 2002, Strauss & Mouradian, 1998, in Vigil-Colet & Codorniu-Raga, 2004). Sergeant,Van De Pool, & Goozen state that impulsivity is connected to reactivity differences of the BAS (1994). This makes sense because the BIS normally inhibits behavior temporarily. An individual with a high BIS threshold may experience an inhibition deficit and even aggression. In fact, Vigil-Colet & Codorniu-Raga have found a correlation between inhibition deficit, anger, and aggression (2004).

The neocortex is also responsible for behavioral inhibition. Critchley, Simmons, Daly, & Russell found in their study of patients with mild mental retardation that violent individuals had significantly lower neuronal density in their prefrontal lobe (2000). If the BIS does not activate, aggression will occur.


Aggression does not have a singular cause. Aggression comes about by an overlap of interrelated behaviors, systems, traits, and biological factors (Cairns & Stoff, 1996). The FFS, BAS, & BIS are part of the reptilian brain and are common to reptiles and mammals – including humans. Our present human species dates back about 250,000 years. This means that the human brain did not evolve to deal with the present day environment (Franken, 2002). The human brain evolved for survival of the species. The systems of the RST are part of that evolution. Although we can use cognition and behavior modification, we still must live with these basal systems – at least until they experience further evolutionary change. All three systems of the RST operate in concert with each other as well as with the individual’s genetic, psychological, and cultural makeup. Malfunction of RST systems can result in light abnormal behavior or even a clinical condition.

However, as O’Neill cautions, biology is not the sole determinant of behavior and biological deficiencies in aggression mediating systems do not predestine an individual to a life of violence (2001). Yet, by understanding the underlying biological systems that mediate aggression, we can better understand why aggression occurs and how it may be prevented. It is clear that a remedy for human aggression and violence can only be found in the collaborative work of biological, psychological, and sociological researchers.


Aggression. (2000). A Dictionary of Biology [Electronic version]. Oxford University Press. Retrieved from Oxford Reference Online database.

“amygdala n.” (2002). Concise Medical Dictionary [Electronic version]. Oxford University Press. Retrieved from Oxford Reference Online database.

Bailey, K. (1987). Human Paleopsychology: Applications to Aggression and Pathological Processes [Electronic version]. Hillsdale, N.J.: Lawrence Erlbaum Associates. Retrieved from Questia database.

Beebe, Lora H. (2003). Theory-based research in schizophrenia. Perspectives in Psychiatric Care [Electronic version], 39(2), 67+. Retrieved from Questia database.

Berkowitz, L. & Harmon-Jones, E. (2004). Toward an understanding of the determinants of anger. Emotion 4(2), 107-130.

Bondar, NP & Kudriavtseva NN. (2003). Effect of the D1-receptor antagonist SCH-23390 on the individual and aggressive behavior in male mice with various aggression experience [English abstract. Article in Russian]. Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova / Rossiiskaia akademiia nauk [Electronic version], 89(8), 992-1000. Retrieved from PubMed database.

Blair, R.J.R. (2004). The roles of orbital frontal cortex in the modulation of antisocial behavior. Brain and Cognition [Electronic version], 55, 198-208. Retrieved from ScienceDirect database.

Cairns, R. & Stoff, D. (Eds.). (1996). Aggression and Violence: Genetic, Neurobiological, and Biosocial Perspectives [Electronic version]. Mahwah, N.J.: Lawrence Erlbaum Associates. Retrieved from Questia database.

Colman, A. M. (2001a). “Limbic system n.” A Dictionary of Psychology (Oxford University Press. Retrieved from Oxford Reference Online database.

Colman, A. M. (2001b). “Mammillary body n.” A dictionary of psychology (Oxford University Press. Retrieved from Oxford Reference Online database.

Colman, A. M. (2001c). “Ascending reticular activating system n.” A Dictionary of Psychology (Oxford University Press. Retrieved from Oxford Reference Online database.

Comings, D., & Blum, K. (2000). Reward deficiency syndrome: genetic aspects of behavioral disorders. Progress in brain research [Electronic version], 126, 325-341. Retrieved from Science Direct database.

Corr, P. (2004). Reinforcement sensitivity theory and personality. Neuroscience and Biobehavioral Reviews [Electronic version], 28, 317-332. Retrieved from ScienceDirect database.

Critchley, H.D., Simmons, A., Daly, E.M., Russell, A., Van Amelsvoort, T., Robertson, D.M., Glover, A., & Murphy, D.G.M. (2000). Prefrontal and medial temporal correlates of repetitive violence to self and others. Biological Psychiatry [Electronic version], 47, 928-934. London, United Kingdom: Society of Biological Psychiatry. Retrieved from Science Direct database.

Field, T. (2002). Violence and Touch Deprivation in Adolescents [Electronic version]. Adolescence 37(148), 735. Retrieved from Questia database.

Fuentes, A. (2012). The Roots of Human Aggression. Retrieved October 3, 2015 from

George, D., Rawlings, R., Williams, W., Phillips, M., Fong, G., Kerich, M., Momenan, R., Umhau, J, & Hommer, D. (2003) A select group of perpetrators of domestic violence: evidence of decreased metabolism in the right hypothalamus and reduced relationships between cortical/subcortical brain structures in position emission tomography. Psychiatry Research: Neuroimaging [Electronic version], 130(1). Retrieved from Science Digest database.

Gray, J. (1991). Fear, panic, and anxiety: What’s in a name? Psychological inquiry 2(1), 77. Retrieved from Questia database.

Guy, D., Hogan, B., & Keltner, N. (2001). Dopaminergic and serotonergic receptor function in the CNS. Perspectives in Psychiatric Care [Electronic version], 37(2), 65. Retrieved from Questia database.

Höglund, E., Korzan, W., Watt, M., Forster, G., Summers, T., Johannessen, H., Renner, K., & Summers, C. (2004). Effects of L-DOPA on aggressive behavior and central monoaminergic activity in the lizard Anolis carolinensis, using a new method for drug delivery. Behavioural Brain Research [Electronic version] (Article in press). Retrieved from Science Direct database.

Lesch & Merschdorf (2000). Impulsivity, aggression, and serotonin: a molecular psychobiological perspective [Electronic version]. Behavioral Sciences & the Law 18(5), 581-604. Retrieved from Science Direct database.

Linnoila, M., Virkkunen, M., Scheinin, M., Nuutila, A., Rimon, R., & Goodwin, F. K. (1983). Low cerebrospinal fluid 5-hydroxyindoleacetic acid concentration differentiates impulsive from nonimpulsive violent behavior. Life Sciences [Electronic version], 33(26), 2609-2614. Retrieved from Science Direct database.

Miczek, K., Fish, E., deBold, J. & deAlmeida, R. (2002). Social and nerual determinants of aggressive behavior: pharmacotherapeutic targets at serotonin, dopamine and y-aminobutyric acid systems. Psychopharmacology [Electronic version], 163 434-458. Retrieved from Science Direct database.

McNaughton, N. & Corr, P. (2004). A two-dimensional neuropsychology of defense: fear/anxiety and defensive distance. Neuroscience and Biobehavioral Reviews [Electronic version]. Retrieved from Science Direct database.

O’Neill, M. (2001). Stalking the mark of Cain. Harvard Journal of Law & Public Policy [Electronic version], 25(1), 31+. Retrieved from Questia database.

Pack, P. (2001). CliffsQuickReview: Anatomy and Physiology. New York: Hungry Minds.

Panksepp, J. (1998). Affective Neuroscience: The Foundations of Human and Animal Emotions [Electronic version]. New York: Oxford University Press. Retrieved from Questia database.

Pontius, A. (2004). Fastest fight/flight reaction via amygdalar visual pathway implicates simple face drawing as its marker: Neuroscientific data consistent with neuropsychological findings. Aggression and Violent Behavior [Electronic version], (Article in press). Retrieved from Science Direct database.

Purves, K., Orians, G., Heller, C., and Sadava D. (2004). Life: The Science of Biology (7th ed.) [Electronic preview version]. Sinauer Associates, Inc., and W.H. Freeman & Co.: New York. Retrieved on February 21, 2004 from life7e_sample_chapters/

Reiner, P. (1995). Are mesopontine cholinergic neurons either necessary or sufficient components of the ascending reticular activating system? Seminars in Neuroscience [Electronic version], 7, 355-359. Retrieved from Science Direct database.

Renfrew, J. (1997). Aggression and Its Causes: A Biopsychosocial Approach [Electronic version]. New York: Oxford University Press. Retrieved from Questia database.

Revelle, W. (1995). “Personality Process.” Annual review of psychology, (46)1. Retrieved from EBSCOhost Psychology and Behavioral Sciences Collection database.

Rodriguiz, RM., Chu, R., Caron, MG., Wetsel, WC. (2004). Aberrant responses in social interaction of dopamine transporter knockout mice. Behavioral Brain Research [Electronic Version], 148(1-2), 185-98. Retrieved from PubMed database.

Sergeant, J., Van De Poll, N., Van Goozen, S. (Eds.). (1994). Emotions: Essays on Emotion Theory [Electronic version]. Hillsdale, N.J.: Lawrence Erlbaum Associates. Retrieved from Questia database.

Siegel, A. & Shaikh, M. B. (1997). The neural bases of aggression and rage in the cat. Aggression and Violent Behavior [Electronic version], 2(3), 241-271. Retrieved from ScienceDirect database.

Summers, C.H., Summers, T.R., Moore, M.C., Korzan, W.J., Woodley, S.K., Ronan, P.J., Höglund, E., Watt, M.J., & Greenberg, N. (2003). Temporal patterns of limbic monoamine and plasma corticosterone response during social stress. Neuroscience [Electronic version], 11(6), 553-563. Retrieved from Science Direct database.

Tyson, P. D. (1988). Physiological arousal, reactive aggression, and the induction of an incompatible relaxation response. Aggression and Violent Behavior, 3, 143-158. Retrieved from Science Direct database.

University of Colorado Health Sciences Center. (1999). Dopamine. Retrieved October 10, 2004, from

Veenema, A., Meijer, O., de Kloet, R., Koolhaas, J., & Bohus, B. (2003).Differences in basal and stress-induced HPA regulation of wild house mice selected for high and low aggression. Hormones and Behavior [Electronic version], 43(1), 197-204. Retrieved from Science Digest database.

Vigil-Colet, A. & Codorniu-Raga, M. (2004). Aggression and inhibition deficits, the role of functional and dysfunctional impulsivity. Personality and Individual Differences [Electronic version.] (Article in press). Retrieved from Science Direct database.

Yao, R., Ramehwar, P., Donnelly, R., & Siegel, A. (1999). Neurokinin-1 expression and co-localization with glutamate and GABA in the hypothalamus of the cat. Molecular Brain Research [Electronic version], 71(2), 149-158. Retrieved from Science Digest database.

Zillmann, D. (1979). Hostility and Aggression [Electronic version]. Hillsdale, N.J.: Lawrence Erlbaum Associates. Retrieved from Questia database.

© 2015 Rosa Malaga


PhilipAr on May 06, 2019:

Corr has updated his definition of aggression in 2016, and taken aggression out of the FFS, which, if you cite Corr (2004), is the FFFS.

FFS is RST (Gray, unknown year).

FFFS is revised-RST (Corr, McNaughton) from 2000.

The factor “fight” has been redefined as “active avoidance” and aggression was made an additional factor. Check

Related Articles