In trying to understand how aggression works, as well as aggressive emotions like anger, I decided to go to the animal literature. Human psychology research is all too prone to being determined by researchers’ preconceptions, and we all have a lot of firsthand experience and personal agendas when it comes to theorizing about human behavior. It’s easier to get some distance when thinking about animals; we have less stake in any particular theory of how animal emotions work. It’s also easier to set up experimental conditions with animals that would be hard to do ethically with humans, like keeping them in confinement and exposing them to stressors.
What the mammal literature says about aggression is that it splits neatly into discrete types. Researchers disagree on exactly how many clusters there are, since there are inevitable judgment calls in defining taxonomies. And the pattern is somewhat different depending on species. But one very consistent finding is that there are qualitatively different types of aggression. They are governed by different hormones, activated in different situations, and seem to involve different subjective experiences.
|Target||Conspecifics, other species, inanimate objects||Conspecifics only||Conspecifics and other species||Other species only|
|Situation||Acute pain, imminent danger without possibility of escape||Competition (over e.g. food, territory, mates)||Threats to nursing young||Hunting edible prey|
|Affect||Distressed, angry, fearful||alert||fearless||Calm, alert, happy, curious, fearless|
|Piloerection||Depends on species||Yes||Yes||No|
|Vocalizing and threats||Yes||Yes||No||No|
|Association with sex hormones||?||Yes (increased by testosterone; blocked by ovarian hormones)||Yes (increased by progesterone, testosterone)||Depends on species|
|Cortisol levels during attack||High||High||Low||Low|
|Other positively associated hormones||cholecystokinin, dopamine, histamine, substance P||ACTH, CRH, histamine, norepinephrine, substance P, vasopressin||NO, vasopressin, oxytocin||acetylcholine|
|Other negatively associated hormones||norepinephrine||serotonin||CRH, neuropeptide Y, neurotensin||serotonin|
|Brain region promoting the behavior||amygdala, hippocampus, PAG||Amygdala, lateral hypothalamus, lateral septum, olfactory bulb||dorsal raphe, lateral septum||amygdala, lateral hypothalamus, olfactory bulb|
|Brain region inhibiting the behavior||lateral septum, medial hypothalamus||?||PAG||PAG|
|Drugs that increase the behavior||amitriptyline, delta-9-THC, desmethylimipramine, ethanol, imipramine, iproniazid, naloxone, nialamide, pargyline||amphetamine, anabolic steroids, chlordiazepoxide, cyproheptadine, ethanol, fenfluramine, PCPA||alprazolam, chlordiazepoxide, diazepam, fluoxetine, oxazepam||arecoline|
|Drugs that decrease the behavior||lithium, opioids, PCP||5-HT, cannabis, citalopram, fluoxetine, fluprazine, naloxone, quipazine, tryptophan||5-HT, amitriptyline, amfonelic acid, desipramine, fluprazine, GnRH antagonists, imipramine, morphine, NOS inhibitors, PCPA||5-HT, amphetamine, atropine, delta-9-cannabidiol, ethanol, scopolamine|
|Effect of domestication||reduces||no change||no change||no change|
“Defensive Aggression”/”Defensive Rage” – Cortisol, Substance P
A certain cluster of behaviors in mammals can be called “defensive aggression”, “affective defense,” or “defensive rage”. These behaviors are reactions to pain or immediate threat, whether that threat comes from a member of the same species, a member of a different species, or an inanimate object.
Defensive aggression is associated with negative emotions like fear and anger. It is aversive; a rat will learn not to push a lever that stimulates its brain in the same region that stimulates defensive aggression. It is also associated with cortisol (the “stress hormone”), substance P (involved in pain perception), cholecystokinin (associated with panic), all suggesting that it is a reaction to frightening and painful situations.
Defensive aggression in some species seems to involve qualitatively different and “milder” types of attack (less likely to cause injury) than other types of aggression. It is also prompted by the same types of situations and same regions of brain stimulation associated with fleeing, hiding, and submission signals (like baring the belly to get an opponent to stop attacking.) And animals engage in defensive aggression reflexively when hurt even when there is no visible attacker; they’ll “attack” inanimate objects or the air, as though “letting off steam”. Speculatively, these details suggest that defensive aggression is something of a reflexive “lashing out” when an animal is hurt or scared, not very well optimized to injure or intimidate an opponent, and have more in common with other self-preservation behaviors (like fleeing, hiding, or submitting) than with other types of aggression.
“Affective Defense”/“Defensive Rage” in Cats
“Affective defense” in mammals typically involves flattening of the ears, lowering of the body, drawing in the head, pupillary dilation, piloerection, hissing, and stiffening of the tail. It is triggered by either a conspecific or a member of another species who is perceived to be a threat.
In cats, “defensive rage” behavior includes ear retraction, piloerection, back arching, pupillary dilatation, vocalization, unsheathing of the claws, and paw strike. It occurs when a cat is threatened by either a member of the same or different species. Stimulating the midbrain periaqueductal gray (PAG), which is generally a pain center, elicits defensive rage behaviors in cats.
Various compounds associated with pain and stress, as well as acute ethanol intoxication, can affect the “defensive rage” response.
Blocking substance P, a substance involved in pain response, in cats reduces the defensive rage response to stimulation in the medial amygdala and medial hypothalamus.
Ethanol enhances defensive rage responses in cats, while it reduces predatory attacks.
Cholecystokinin, a neuropeptide and digestive hormone which causes nausea and induces panic when administered to humans, potentiates the defensive rage response in cats.
Naloxone reduces the threshold for inducing defensive rage in the cat by brain stimulation; opioid receptor agonists block defensive rage.
Defensive rage in cats appears to be inhibited by the medial hypothalamus. Medial hypothalamus lesions make cats extremely defensive – they spit and claw in the presence of humans, they’ll run from a dog and fight if attacked. However, olfactory bulbectomy doesn’t affect defensive aggression in cats.
Defensive Aggression in Dogs
The septal region in the brain is involved in inhibiting defensive aggression in dogs. Septal lesions make dogs more “overexcitable, baring their teeth, and attempting to bite when handled.”
Cortisol-Related Aggression in Hamsters
Syrian and Siberian hamsters are more aggressive in the winter (short-day condition) than the summer, despite their testes being smaller in the winter. The increased aggression appears to be mediated by elevated cortisol, downstream of melatonin signaling. In primates as well, seasonal rises in testosterone don’t always correlate to increased aggression, and exogenous T doesn’t always increase aggression. Just as in male humans, there is no correlation between testosterone levels and aggressive behavior.
However, amygdala lesions suppress shock-induced fighting in hamsters.
Defensive Aggression in Marmosets
As with cats and opossums, stimulating the marmoset ventromedial hypothalamus elicits aggressive responses, chiefly short attacks and vocal threats, as well as flight responses.
Female marmosets attack intruders; the magnitude of the aggressive response correlates positively with testosterone level immediately after the attack.
Defensive Aggression in Mice
Defensive aggression in mice seems to be inhibited by the septal region of the brain and enhanced by the olfactory bulb, unlike hamsters and gerbils who do not have an olfactory bulb-dependent aggression response.
Mice who have had their olfactory bulb removed do not fight back when attacked or exhibit fighting behavior after electric shocks. Peripheral anosmia does not cause this response, indicating that its effect on aggression is not due exclusively to the fact that it is necessary for smell.
Septal lesions in mice enhance defensiveness; struggling, biting, and escaping.
Defensive Aggression in Rabbits
Septal lesions increase defensive responses (like foot thumping) to human experimenters in rabbits.
Defensive Aggression in Rats
Defensive biting in rats is different from attack biting; it is usually targeted at the snout, while attacking rats bite their opponent’s back; and defensive biting is seen more often against human hands or tools than against rats. Defensive biting only occurs during or immediately after the defending animal has been hurt, and only when escape is impossible. Defensive biting also does not involve piloerection, while offensive biting always does.
Defensive aggression is specifically selected against when rats are domesticated.
233 wild-caught rats were selected for “tameness”, that is, lower rates of aggressive behaviors towards human handlers, or “aggression”, that is, higher rates of aggressive behaviors towards human handlers, over 8-10 generations. 
There was no difference in testosterone levels between tame and wild rats of both sexes; however, aggressive rats had significantly higher serum cortisone levels than wild rats, in both sexes. Aggressive rats had significantly larger startle responses to stimuli than tame rats, in both sexes.
Tame rats show fewer displays of defensive aggression towards other rats than aggressive rats, but no fewer displays of offensive aggression.
As with other animals, the septal and medial hypothalamus regions of the brain appear to inhibit defensive aggression in rats, while the amygdala and hippocampus stimulate it.
Septal lesions in rats enhance defensiveness – heightened fighting in response to foot shock and handling. Medial hypothalamus lesions also dramatically increase defensiveness. Amygdala and hippocampus lesions, by contrast, decrease defensiveness.
Certain drugs affect defensive aggression in rats.
“Irritable aggression” in both male and female rats – an increased tendency to fight each other when deprived of food or sleep or administered electric shocks – is increased by administering cannabis or delta-9-THC.
Lithium reduces aggression in rats in response to pain from hot plates or electric shocks.
The tricyclic antidepressant drugs imipramine, amitryptiline, and desmethylimipramine, and the MAOIs nialamide, iproniazid, and pargyline, all increased shock-induced aggression in rats.
Acute administration of dopamine intravenously increases shock-induced aggression in rats, while acute intravenous norepinephrine reduces it.
Phencyclidine (PCP) dose-dependently reduces defensive aggression in rats both against other rats after foot shock, and against an inanimate target after immobilization and tail shock.
Histamine increases rat aggression in response to foot shocks; this effect is further potentiated by an H1-receptor-blocking antihistamine and suppressed by an H2-receptor-blocking antihistamine, suggesting that H2 histamine receptors are involved in defensive aggression.
Cholecystokinin type 2 receptors in the PAG are necessary for two defensive behaviors in rats, freezing and escape.
Pain-Induced Aggression in Spider Monkeys
Spider monkeys will bite other monkeys, rats, mice, dolls, and balls immediately after being administered painful electric shocks. If two monkeys are both shocked, initially both will attack; after repeated shocks, a pattern emerges where one always attacks and one always flees.
Aggressive Vocalization and Pain-Induced Aggression in Squirrel Monkeys
The “kecker” call, associated with aggression, can be stimulated in squirrel monkeys by electrodes in the amygdala, hypothalamus, and periventricular gray.
Phencyclidine at high doses blocks pain-induced aggression in squirrel monkeys.
Social Aggression (“Offensive Aggression”, “Intermale Aggression”) – Testosterone, Vasopressin, Low Serotonin
Social aggression, unlike defensive aggression, is directed only at members of one’s own species. It is sometimes called “intermale aggression” or “hormone-dependent aggression” even though it is not exclusive to males, because it is generally more common in males and correlates well to testosterone levels. It also inversely correlates to serotonin levels.
Social aggression revolves around competition for scarce resources – mates, territory, or in some species food and water. It generally involves threat displays intended to make an opponent back down without a fight.
Social aggression is the least well-categorized of the types of aggression I describe here; in some species (such as marmosets) there doesn’t seem to be a clear distinction between social and defensive aggression. In rats, social aggression is always accompanied by piloerection (hair standing on end) while defensive aggression never is. But not all species seem to have this sharp distinction.
There are major differences between the ways “social aggression” is studied in rodents vs. primates which make the situation more confusing.
In rodents, “offensive aggression” is defined as the propensity for an individual to attack an unknown intruder into his space. Since the “resident” invariably defeats the “intruder”, dominance and “offensive aggression” are identical. Dominant rodents are higher in testosterone than average and have more access to mates. In rodents, the relationship between social aggression and the hormones serotonin and testosterone is straightforward: testosterone raises social aggression and serotonin lowers it. Stress and anxiety anticorrelate with offensive aggression.
In primates and social carnivores such as wolves and mongooses, however, studies are typically done within a group of individuals who live together (in the wild or the lab). Conflicts are primarily with community members, and only occasionally with strangers. And intragroup conflicts often resolve with little or no physical violence, just threat behaviors and mild scuffling. So “dominance” is a more complex phenomenon; a dominant individual in a group is the one who wins most conflicts and receives the most submission behavior, and has the most access to resources (like mates, food, and water), but the dominant individual is not necessarily the most aggressive individual.
The relationship between dominance, aggression, and the hormones testosterone, serotonin, and cortisol, is likewise complicated in primates and in social carnivores. Dominance rank does not necessarily correlate positively with aggression. Completely nonviolent individuals are, by definition, at the bottom of the dominance hierarchy (they lose all fights they’re in), but otherwise, in primates and carnivores, “fighting more” is not necessarily “winning more.” The most dominant individuals in a stable hierarchy are rarely threatened, and can easily cause others to back down with a harmless threat display.
Aggression does not always correlate with cortisol in primates and social carnivores. Dominance usually correlates positively with baseline cortisol levels. On the other hand, losing fights causes an acute spike in cortisol in the loser. Because of the negative feedback in cortisol levels, these two observations are consistent; frequent experiences of losing fights can be expected to depress long-term baseline cortisol levels, even as each losing battle causes a spike in cortisol in the short term.
Serotonin in primates correlates positively with dominance rank and with non-severe aggression (initiating threat displays or harmless physical scuffles) but negatively with severe aggression (wounding another primate). As in rodents, low serotonin correlates with serious violence in primates, but primates also have a more complex repertoire of dominant/threatening social behavior which are associated with high serotonin.
Testosterone, though, in primates and carnivores just as in rodents, has a straightforward positive correlation with both dominance and aggression.
Social Aggression in Baboons
Among female baboons, testosterone correlates with dominance rank and within-individual aggression but not across-individual aggression – i.e. higher-T baboons are not more aggressive overall, but particular baboons are more aggressive at times when their T is higher.
Dominant baboons have more copulatory success, are more likely to dominate in conflicts (receive submissive gestures or avoidance from other baboons), and are more likely to win conflicts over food. But they do not engage in more aggressive encounters. High dominance rank among baboons is associated with low baseline cortisol and high cortisol response to stress.
Social Aggression in Chimpanzees
Behavioral style in chimpanzees was broken down into 6 principal components:
- “Smart” (uses coalitions when initiating aggression; is usually the groom-ee in grooming interactions; has most play offers accepted)
- “Affiliative” (participates in a lot of grooming; frequent hugging and touching)
- “Playful” (plays often and with many other chimps)
- “Aggressive” (most social interactions are aggressive; has many coalition partners in aggression)
- “Friendly” (has many friends; spreads affiliative behavior around many individuals)
- “Mellow” (frequently does not react to aggression or social approach)
“Friendly” and “Affiliative” personality was not associated with dominance rank.
“Playful” and “Smart” personalities were more likely to be subordinate.
“Aggressive” and “Mellow” personalities were more likely to be dominant.
Cortisol did not correlate with rank, aggression given, or aggression received. There was a nonsignificant positive association between cortisol and the “Smart” and “Aggressive” styles.
In adolescent male chimpanzees, testosterone (after correcting for age) was positively associated with dominance and aggression given, negatively associated with aggression received, and positively associated with the “mellow” behavioral style. Testosterone was not associated with the “Aggressiveness” behavioral style. Note that “Aggressiveness” indicates that a high percent of one’s total social interactions are aggressive, so an individual who is both aggressive and friendly might have a low “Aggressiveness” score.
Dominance rank, aggression, and testosterone are correlated in adult male chimpanzees.
Citalopram, an SSRI, reduced aggressive behavior in a zoo chimpanzee.
Aggression and Social Dominance in Cynomolgus Monkeys
Dominant cynomolgus monkeys (those who win most conflicts) tend to also engage in more aggression overall. Serotonin tends to inhibit aggression.
Other hormones have relationships with aggression and dominance as well: testosterone is positively correlated with dominance rank; cortisol is positively correlated with rank in males but not females; and ovariectomy increases both aggression and submission in females, suggesting that some ovarian hormone is responsible for blocking aggression and submission.
In female cynomolgus monkeys, the lower the social rank of a monkey, the more aggression she received and the more submissive behaviors she practiced. But aggressive behaviors follow an inverted U-shaped relationship with rank; the most dominant individuals actually engage in less aggression than the middle ranks, though the most subordinate individuals do the least aggression of all. If monkeys are split into two groups, “dominant” and “subordinate”, the difference in aggression is not significant, but it’s clear how with this pattern, different choices of split point would result in different conclusions.
Dominant monkeys were larger and had higher levels of LH, cortisol response, oxytocin, and dopamine metabolites than subordinates.
There was no association between cortisol levels and social rank in female cynomolgus monkeys. Higher-ranked monkeys engaged in more aggression while lower-ranked monkeys engaged in more submission.
When given sertraline, an SSRI, adult female cynomolgus monkeys showed changes in social behavior. Before treatment, dominant monkeys were more aggressive than subordinates; with sertraline, dominant monkeys engaged in less aggression until they matched the low subordinate level. Before treatment, subordinate monkeys engaged in more submission than dominants; with sertraline, the subordinates’ submissive behavior dropped to match the low dominant level.
Homovanillic acid levels (a metabolite of dopamine) were higher in both male and female dominant cynomolgus monkeys than in subordinates. No association with norepinephrine metabolites. In males but not females, lower HIAA (a metabolite of serotonin) was associated with dominance.
Dominant male monkeys have higher basal cortisol and testosterone levels; subordinate monkeys have stronger cortisol response to ACTH challenge.
Ovariectomy causes a 2-3x increase in aggression and submission in female cynomolgus monkeys.
As with other animals, ethanol can stimulate aggression in cynomolgus monkeys.
Acute and chronic alcohol drinking both increase rates of contact aggression in cynomolgus monkeys.
Social Aggression in Dogs
Domestic dogs who engaged in “leash aggression” (attempting to attack other dogs while on leash) were matched to a dog of the same age, sex, and breed who did not engage in “leash aggression.” Aggressive dogs were more likely to bark, lunge, and growl at model dogs than non-aggressive dogs. Aggressive dogs had higher levels of free vasopressin than nonaggressive dogs, but no difference in oxytocin.
Among assistance dogs bred for affectionate dispositions and low aggressiveness, oxytocin was higher than in pet dogs.
Social Aggression in Gerbils
Like mice and rats, male gerbils who cohabit with a female will attack unfamiliar intruders in their home territory. Castration abolishes territorial aggression; castration + supplemental testosterone restores it.
Olfactory bulbectomy reduces social aggression in gerbils; high dose testosterone propionate reverses this effect. 
Gerbils will typically attack unfamiliar gerbils and also rats and mice that venture into their territory. Gerbils dosed with delta-9-THC will still sniff, approach, and chase a mouse, but will not bite it.
Social Aggression in Hamsters
As with other animals, testosterone and other androgens increase aggression in hamsters; so do the hormones vasopressin and corticotropin releasing hormone (CRH), a stimulator of the HPA-axis.
In hamsters, vasopressin administration increases rates of flank marking (a dominance behavior), and vasopressin antagonists reduce flank marking by dominant hamsters, which in turn increases flank marking by submissive hamsters.
Blocking vasopressin dose-dependently reduces male hamsters’ rate of attacking intruders.
A CRF1 antagonist blocks attacks against intruding male hamsters – higher latency to bite, lower chase duration, lower attack frequency.
Anabolic steroids (testosterone cypionate, nandrolone deconate, and boldenone undecylinate) increase offensive aggression in male hamsters.
Social Aggression in Marmosets
Common marmosets exhibit “vocal threats” along with limited piloerection in the tail and relatively harmless “short attacks”, when competing over food. Short attacks are generally made against lower-ranking or younger monkeys, are terminated by flight or submissive squeals, and are never followed by chasing.
Genital display and flicking of the ear-tufts are behaviors that alpha marmosets usually make towards subordinate marmosets, or any marmosets towards strange marmosets and humans. If the strangers counter-threaten, serious biting attacks ensue. Violent attacks and fighting are accompanied by substantial piloerection.
In the common marmoset and black tufted-ear marmoset, as well as in lemurs and tamarins, dominant individuals have higher cortisol than subordinates.
Social Aggression in Mice
Olfactory bulbectomy reduces social aggression in mice; peripherally induced anosmia does not.
Naloxone suppresses intermale aggression in isolated mice.
Cannabis reduces the tendency of mice to fight an intruder, even at doses too low to suppress locomotor activity.
In a subpopulation of rats and mice, roughly a quarter of subjects, ethanol administration increases aggression against intruders. In particular, ethanol lengthens the duration of bursts of aggressive activity, but does not affect the latency to attack.
Mice lacking the HNMT gene have higher levels of brain histamine, and are more aggressive against intruders. They also have an altered sleep/wake cycle (they are more active during the light period when mice usually sleep, and less active during the dark period when mice are usually awake.)
Mice lacking substance P receptors are far less likely to attack an intruder.
Social Aggression in Rabbits
The male rabbit who is most likely to follow, attack, and chase is considered the dominant rabbit in a group; he has higher peripheral testosterone levels than the others.
“Offensive” or “Hormone-dependent” Aggression in Rats
Offensive aggression in rats is clearly delineated from defensive aggression.
In a colony of rats, if an intruder enters, one male rat will typically attack the intruder; this male is also the dominant rat in “agonistic encounters” within the colony. These attacks are preceded by approach, sniffing, and (if the rat is not a colony member) piloerection, followed by biting, boxing, and climbing on top of the other rat. The intruder rat rarely bites back after being attacked.
Only hormone-dependent aggression in rats is accompanied by piloerection; defensive and predatory aggression are not. Hormone-dependent aggression is not territorial – a male rat will attack an unfamiliar male rat even if he is in an unfamiliar area.
When a cat smell is added to a rat cage, offensive attacks disappear; defensive biting is unchanged or increased, however.
Offensive aggression in rats is associated with testosterone, copulation, and winning fights; it is reduced when a rat experiences “disappointment”, failing to get an expected reward.
Castration reduces social aggression in male rats, and testosterone supplementation increases it. The amount of aggression in intact male rats correlates with the baseline level of serum testosterone. Rat testosterone spikes after exposure to a receptive female and after successful aggression.
Male rats will exhibit much more social aggression if they cohabit with females. Both male and female rats will exhibit more hormone-dependent aggression if they are competing for scarce food.
Offensive aggression in male rats increases after copulation with females.
Male intruder rats display offensive aggression against female residents, but never males. Female intruder rats rarely are attacked, and when they are it is usually only after they rebuff multiple attempts to mate.
When access to food or water is restricted, the “alpha” male or female rats in a colony (those who attack intruders the most) are not the same rats who get the most access to the food or water. But alpha male rats are the ones who have the most access to copulating with females.
Rats surprised by a lack of reward in a situation that normally provides rewards show a reduction in social aggression and a greater propensity to be attacked.
Social aggression in rats also anti-correlates with serotonin and is increased by serotonin-depleting drugs and decreased by serotonergic drugs.
Male Wistar rats treated with PCPA, a drug which depletes cerebral serotonin, or a saline control, before being placed in another weight-matched rat’s cage. The PCPA-treated intruder rats frequently attacked the residents; the control rats never did. PCPA-treated rats were also more likely to socially approach the resident rats. Defensive and submissive behaviors were unchanged.
When it was the resident rats who were treated with PCPA or control, treated rats attacked more; there was no change in defensive or submissive behaviors.
Hypothalamic stimulation prompts rats to attack other rats (male and female), anaesthetized or dead rats, and mice, but not toy rats. Castration increases latency of hypothalamic aggression; testosterone reverses the effect. Serotonin-receptor-binding drugs such as fluprazine, quipazine, and TFMPP, increase the threshold for hypothalamic aggression.
Perhaps surprisingly, though, social aggression in rats anticorrelates with anxiety. Rats bred for low rates of anxious behavior were more aggressive than rats bred for high rates of anxious behavior or rats without selective breeding.
Social Aggression in Mongooses
In the dwarf mongoose, dominant females have higher cortisol levels than subordinate females.
Unusually among social mammals, mongooses don’t show elevated testosterone in situations of conflict. Testosterone levels in male mongooses don’t correlate with rates of aggression, dominance rank, or mating rates. 
Mongooses are unusual in that they are cooperative breeders; only a few individuals in a group reproduce, and the rest are “helpers” who look after the children. However the “helper” males have just as much testosterone as the dominant males. Mongooses also continue to play even as adults, which many species don’t.
Social Aggression in Oryx
Oryx engage in postural threats (erect posture, threatening with horns) and head-butting conflicts with the horns of other males. They submit by bowing their heads or leaving after challenged. Melengestrol acetate, a progestin, reduces aggression when given in the feed of a herd of male oryx. Melengestrol reduces testosterone levels, as well as levels of posturing, contact, chasing, and submission.
Social Aggression in Rhesus Monkeys
In rhesus monkeys, serotonin is negatively associated with intra-species aggression in rhesus monkeys, but positively associated with dominance. When aggression is split into the two categories of competitive aggression (threatening, chasing, and displacing, without causing serious injury) vs. severe aggression (causing wounds), we find that serotonin, and dominance rank, are positively associated with competitive aggression and negatively associated with severe aggression.
Testosterone is positively associated with aggression. Cortisol is negatively associated with threat displays.
In free-living young male rhesus monkeys, ACTH and norepinephrine levels were positively associated with aggressiveness ratings, while 5-HIAA (a serotonin metabolite) levels were negatively associated.
28 young male monkeys taken from 3500 free-living macaques on an island in South Carolina were rated for “aggressiveness” by researchers based on direct observation, examination of scars and wounds, and photographs. ACTH was significantly positively associated with aggressiveness, as was norepinephrine; serotonin was negatively associated.
Dominance among females in a free-living macaque colony is associated with the frequency of threatening, displacing, and chasing behavior, but not with severe aggression or spontaneous wounding. High dominance rank correlated positively with 5-HIAA (a serotonin metabolite.) Severe aggression or wounding correlated negatively with 5-HIAA.
The C77G polymorphism in the mu-opioid receptor gene in macaques is associated with an abnormally low cortisol response to stress and pain. Threat displays, such as teeth-baring, staring, and ear-flapping, correlated negatively with cortisol levels. The mutant macaques had significantly higher rates of threat display, but not more cage-shaking or attacks on self or inanimate objects.
Testosterone in male rhesus monkeys correlates positively with rates of aggression, dominance rank, rate of receiving submission, and “tension” (yawning, teeth grinding, and banging objects; also symptomatic of inhibited aggressive behavior due to the presence of dominant animals.) High testosterone correlates negatively with submissive behaviors. On the other hand, the reverse correlation does not apply; the monkeys most likely to submit do not have the lowest testosterone.
Dominance in rhesus monkeys seems to involve activity in the amygdala and lateral hypothalamus.
If you remove the amygdala from a dominant rhesus monkey, he becomes submissive, never aggresses or retaliates, and moves to the bottom of the dominance hierarchy. He also becomes more aggressive/fearless in individual-cage settings.
Stimulation of male rhesus monkeys in the lateral hypothalamus prompts them to aggressively attack the dominant monkey. The stimulated monkeys did not attack females or inanimate objects. The stimulated subordinate monkey usually lost fights with the dominant; the dominant monkey mounted the female more and actively threatened the stimulated subordinate male. Eventually the formerly subordinate monkeys became dominant; their hair stood on end, they strutted, they looked dominant, while the formerly dominant monkeys crouched and had matted hair.
When amphetamine is administered to stumptail macacques, affiliative behavior decreases and aggressive behavior increases.
Social Aggression in Squirrel Monkeys
Squirrel monkeys make threat displays and aggressive vocalizations when faced with a strange intruder; the rate of these aggressive responses increases when they are given ethanol or the benzodiazepine chlordiazepoxide.
Dominance in Vervet Monkeys
Dominance is measured by how often a male monkey succeeds in agonistic encounters (i.e. the other monkey submits or avoids). 36 adult male vervet monkeys were separated into 12 groups of 4. In each, a dominant male (winning over 85% of encounters) emerged. Tryptophan and fluoxetine (both serotonergic) significantly increased the frequency of approaching, proximity, and grooming but decreased the rate of aggressive behaviors. By contrast, fenfluramine and cyproheptadine (which deplete serotonin), decreased approaching, proximity, and grooming and increased aggression.
The animals treated with serotonergic drugs became dominant and remained so; the animals treated with anti-serotonin drugs became subordinate and remained so. This suggests that low serotonin may be a signal of low or threatened dominance, which prompts aggression.
Cortisol levels do not correlate with social dominance in stable groups of vervet monkeys. Cortisol levels rise during competition for dominance among familiar males, particularly among the winners of such competitions.
Social Aggression in Wolves
Cortisol is higher in dominant wolves than subordinate wolves, consistent across 3 packs and 2 years. There is no overall correlation between cortisol and levels of agonistic and aggressive behavior. However, cortisol is higher during the mating period, and so is aggressive behavior. Dominant wolves do not fight more than subordinate wolves; they just win a higher percentage of their fights.
Male wolves are more likely than female wolves to fight against other packs; male wolves also have higher cortisol than female wolves.
Dominant male wolves have higher testosterone and cortisol than subordinate wolves.
Maternal Aggression: Oxytocin, Vasopressin
Maternal aggression is the propensity of mammalian mothers to become more aggressive in defense of their offspring during pregnancy and while nursing.
Maternal Aggression in Mice
Mouse maternal aggression is promoted by nursing and caring for infant offspring, not necessarily pregnancy or even female sex. The male sex hormone testosterone, in addition to pregnancy-related female hormones, increases maternal aggression.
In a species of mice where fathers as well as mothers have significant parental investment into raising children, there is a “paternal aggression” phenomenon in which male parents are more aggressive towards intruders than male virgins are.
Prenatal testosterone exposure increases maternal aggression in mice.
Mouse maternal aggression is blocked by stress, as well as stress and anxiety-related hormones, such as CRH, neuropeptide Y, and neurotensin.
Corticotropin-releasing hormone, as well as the presence of stressors, inhibits maternal aggression in mice. Nursing mice also show reduced fear and anxiety.
Mice selected for high maternal aggression have reduced neuropeptide Y expression, which also correlates with decreased fear and anxiety. They also have increased CRF binding protein expression (which reduces the effect of CRF), and increased NO synthase. 
Neurotensin injected into a lactating mouse’s brain significantly and dose-dependently reduces maternal aggression. Neurotensin antagonists significantly increase maternal aggression. Neurotensin has many functions, including stimulating ACTH production.
Serotonin-related drugs also affect maternal aggression in mice, though the pattern of effect is not obvious.
PCPA, a serotonin depletion agent, as well as 5-HTP, a serotonin precursor, inhibit maternal aggression in postpartum mice. Antagonists of serotonin receptors such as mianserin, methiothepin, and methysergide, also reduce maternal aggression. 5-HTP and PCPA have opposite effects on serotonin but they both increase dopamine levels, and also increase levels of 5HIAA, the metabolite of serotonin.
Imipramine, a tricyclic antidepressant with strong effects on many neurotransmitter receptors, reduces maternal aggression in mice.
Morphine reduces maternal care for pups and maternal aggression in mice.
Maternal Aggression in Rats
Maternal aggression in rodents, like predatory aggression and unlike social aggression, is not accompanied by a cortisol response, elevated arousal, or social signaling (threats). Maternal aggression tends to attack more vulnerable body parts (the belly) as opposed to social aggression (which attacks the back) or defensive aggression (which attacks the face).
Female rats become more aggressive against unfamiliar rats during pregnancy, after birth, and during lactation. To a lesser extent, cohabiting with even a sterile male induces increased aggression in female rats.
Female social aggression in rats is confined to the living area, unlike social aggression in male rats; a female rat outside her home will not attack a stranger.
Female rats need to be stimulated by suckling pups in order to have maternal aggression. Removing nipples doesn’t remove the aggression, but anaesthesia to the ventral skin does, suggesting that the trigger is sensory rather than lactation-related.
Lactating female rats, but not alpha male rats, will bury an intruder after attacking it. Like social aggression and unlike defensive aggression, piloerection is present in both maternal and alpha male attacks on intruders.
Maternal aggression in rats is enhanced by oxytocin and vasopressin, as well as GnRH (which increases the release of sex hormones).
Blocking oxytocin chemically reduces maternal aggression in high-aggression lactating rats, and adding IV oxytocin increases maternal aggression in low-aggression lactating rats. Likewise, blocking vasopressin in high-aggression lactating rats reduces maternal aggression, while IV vasopressin in low-aggression lactating rats increases maternal aggression.
GnRH antagonists reduce maternal aggression in rats, but not maternal care.
Serotonin has a complicated relationship with maternal aggression in rats.
Lesions to the serotonin-producing cells in the dorsal raphe reduce both maternal aggression and maternal care in rats, indicating that serotonin is necessary for maternal aggression.
Also, fluoxetine (an SSRI) increases maternal aggression in rats relative to controls.
On the other hand, serotonergic drugs often decrease maternal aggression, such as fluprazine , amitriptyline, and desipramine.
In keeping with the finding that stress anticorrelates with maternal aggression, all benzodiazepines (which have anxiolytic effects) increase maternal aggression in rats.
The lateral septum is necessary for maternal aggression in rats, and the periaqueductal gray (PAG) inhibits it, as one would expect for a behavior that is negatively associated with anxiety.
Lesions to the lateral septum in rats abolish maternal aggression, as well as maternal behavior such as retrieving, licking, and nursing pups.
Rats lesioned in the periaqueductal gray (PAG) attack intruders 2x as often as controls.
Domestication does not inhibit maternal aggression; wild and domesticated Norway rat strains show no difference in maternal aggression.
Maternal Aggression in Voles
A nitric oxide synthesis inhibitor reduces maternal aggression in prairie voles.
Prairie voles are monogamous, and after pair-bonding, male prairie voles become much more aggressive against intruders. Vasopressin receptor antagonists prevent this increase in aggression, while supplemental vasopressin increases it.
It’s possible that male aggression in voles actually is a closer hormonal match to maternal aggression given the pair-bonding aspect. Consistent with this hypothesis, supplemental testosterone does not increase aggression in male voles and castration does not inhibit aggression.
Predatory aggression is violence against edible prey. It is almost always directed against members of a different species, though some mutations make animals attack conspecifics in ways that resemble predatory aggression.
Predation is distinct from social and defensive aggression in that it is stealthy (there is no vocalization or threat display, to avoid scaring off the prey) and it is pleasurable rather than stressful to the predator. Predatory behavior is not associated with cortisol response, and it is stimulated by the centers of the brain associated with reward and alertness, rather than the ones associated with fear and pain.
Predatory Aggression in Baboons
Olive baboons hunt occasionally, mostly hares, gazelles, birds, and other ungulates. Male olive baboons do most of the killing and eating of prey.
Predatory Aggression in Cats
Cats can attack other animals in two obviously distinct ways; “affective attack”, which involves hissing, growling, back arching, and piloerection; and “predatory attack”, in which the cat quietly stalks its prey and does not make aggressive noises or arch its back, and its hair does not stand on end.
Cats who are quicker to attack rats are also quicker to approach novel stimuli and slower to avoid threatening stimuli; the reverse is true of cats who are slow to attack rats. Predatory behavior in cats seems to be related to curiosity and fearlessness.
Predatory aggression in cats is stimulated by activity in the lateral hypothalamus and amygdala and inhibited by activity in the periaqueductal gray.
Electrical stimulation of the lateral hypothalamus in the cat (the same area that promotes feeding and wakefulness behavior) elicits predatory aggression.
Cats lesioned in the amygdala stop killing mice.
Lesions in the periaqueductal gray (PAG) lowered the threshold to cats attacking rats when stimulated in the hypothalamus.
Gonadectomy in female cats makes them quicker to attack a rat; gonadectomy in male cats makes them slower to attack a rat. This suggests a positive association between testosterone and predation in cats.
The muscarinic agonist arecoline can induce biting attack in the cat; muscarinic antagonists such as scopolamine and atropine block this effect. Arecoline is the psychoactive ingredient in betel nuts, and in humans causes an effect similar to nicotine – alertness, energy, euphoria, and relaxation.
Predatory Aggression in Chimpanzees
There is significant overlap between intraspecific aggression and predation in chimpanzees. They sometimes stalk each other before attacking, and they have been known to eat infant chimpanzees after a fight.
Predatory Aggression in Foxes
Administration of 5-HT (serotonin) significantly reduced a fox’s likelihood of attacking a rat placed in its cage.
Predatory Aggression in Mice
Mice kill and eat crickets. A strain of mice bred for large amounts of voluntary wheel-running had no significant difference from controls in their rates of intermale aggression or maternal aggression, but the wheel-running mice were quicker to attack crickets. Since wheel-running is a pleasurable activity that mice seek out, this suggests that propensity to kill crickets is associated with reward from active behaviors. The wheel-running mice were smaller and had more pups than the control mice; serum testosterone levels were the same.
The reproductive and hormone status of female mice does not correlate with their propensity to attack crickets, suggesting that predatory and maternal aggression have different physiological bases. Ovariectomy reduces maternal aggression in mice but does not reduce cricket-killing.
A mouse’s sense of smell seems related to its ability to distinguish its own species from others. Abolishing it doesn’t reduce predation, but does cause cannibalism (a mouse “preying” on its own kind.)
Experimentally induced anosmia reduces both maternal aggression and intermale aggression, but not cricket-killing.
Olfactory bulbectomy in mice causes cannibalism – one adult mouse will kill and eat the other, and mothers will eat their young.
Similarly, the hormone vasopressin in mice seems to be essential for aggression against other mice, but not for predation against other species.
Mice with a disrupted vasopressin receptor, Avpr1b-/-, have lower intermale aggression, maternal aggression, and defensive biting responses, but the same number of “defensive avoidance” behaviors (fleeing, boxing). Predatory aggression against crickets is intact in Avpr1b-/- mice. This gene seems to be required for all types of attack responses towards conspecifics, but not to other species.
Some neuroactive drugs block mouse predation, including drugs that increase serotonin.
Amphetamine, imipramine, and tripelennamine (an antihistamine) block mice from killing frogs. Serotonergic drugs (imipramine, fluoxetine, 5-HT) inhibit locust-killing in CBA mice.
Predatory Aggression in Minks
If you put a rat in a mink’s cage, it will attack 100% of the time. When given 5-HT (serotonin), only half the minks attacked the rat.
Predatory Aggression in Primates
Many species of primates engage in some predation, against frogs, lizards, snakes, birds, or monkeys. Almost all use the craniocervical bite, a killing bite to the head or neck of the prey. The exception is the baboon, which often starts to eat before its prey is dead, perhaps because the baboon’s size and strength allow it to immobilize prey even without immediately killing it.
Predatory Aggression in Rats
Rats often kill and eat frogs and turtles. Attacks on these animals are probably a better measure of rat predatory aggression than mouse-killing, even though rats do often eat mice as well; mouse-killing seems stimulated by some of the same mechanisms as social aggression and is a less “pure” instance of the class.
Testosterone doesn’t affect predatory aggression in rats.
When male Wistar rats were tested for whether they would kill a frog (Rana pipens) placed in their cage, those who didn’t kill the frog immediately never attacked a frog on subsequent trials. Testosterone injection didn’t induce frog killing. The rats who did kill frogs learned to kill them faster upon repeated trials, but again testosterone injection had no effect on latency.
Testosterone supplementation doesn’t increase frog-killing in female rats either.
Some drugs also reduce predatory aggression in rats.
Amphetamine blocks rats from killing mice, and not just because it reduces appetite; at low doses, rats are still willing to kill mice even though they don’t want to eat them. The same is true for frog-killing.
Delta-9-cannabinol (the main psychoactive ingredient in cannabis) reduces rats’ frequency of attacking turtles.
Some rats attack other rats in ways more akin to predation than social aggression.
In strains of rats with abnormally low glucocorticoid function, the lateral hypothalamus is activated during conflicts with other rats. These low-cortisol rats attack other rats on the head, throat, and belly, without any of the usual preliminaries of signaling aggression. In other words, their aggression against conspecifics looks more like predation. Humans diagnosed with antisocial personality disorder also have lower cortisol levels than average.
Rats subjected to post-weaning social isolation also are abnormally aggressive and prone to attack vulnerable regions without intention signaling, again more like predatory or maternal aggression than typical social aggression.
As with social aggression and maternal aggression, domestication of rats does not reduce predatory aggression. Norway rats bred for low aggression towards humans did not show any decline in predatory behavior.
Predatory Aggression in Voles
After 13 generations of selecting bank voles for higher rates of predatory behavior, raising the rate of predatory behavior 5x relative to controls, the two highest SNPs found in the predatory lines were in the gene PDE4D, found expressed in the brain. PDE4D is responsible for degrading cAMP. PDE4D inhibitors have antidepressant effects.
Mobbing refers to behaviors by groups of prey animals to approach, intently observe, harass, and attack a predator or other large member of another species. Mobbing is common in primates, particularly New World monkeys.
Baboons, geladas, and chimpanzees launch aggressive counterattacks that can seriously wound predators; e.g. baboons often kill leopards. Arboreal New World monkeys like tamarins and capuchins, by contrast, tend to lunge, jump, and make stereotyped threat behaviors when a predator (such as a snake) has captured one of them. Where mobbing does not pose a lethal threat to the predator, it may be an attempt to get the predator to move on, as well as monitoring the threat. But capuchins also mob non-threatening, non-prey animals, and the reason why is unknown.
Parallels to Human Aggression
The criminology literature tends to make a single distinction in types of aggression – “reactive” aggression, a spontaneous, “hair-trigger” loss of self-control in response to frustration or provocation, or “predatory” aggression, a deliberate behavior engaged in to achieve a desired goal. Acts of “reactive” aggression are done under stress; acts of “predatory” aggression are done calmly and strategically, and may even be enjoyable. The analogy between “predatory” aggression in humans and literal predation in animals is loose, and based primarily on the fact that both involve low cortisol and are not associated with strong negative emotions.
“Reactive” aggression in this criminology paradigm would seem to correspond either with “defensive” or “social” aggression – they’re not clearly delineated.
Children with a history of aggressive behavior have been observed to cluster into two types. One type of child engages only in “impulsive” or “reactive” aggression. A second type of child engages both in this “impulsive” aggression and in “premeditated”/ “pro-active” aggression.
Children in the “impulsive” group were more likely to have low IQs and schizophrenia diagnoses; children in the “mixed” group were more likely to have a history of drug abuse. 
In studies of juvenile offenders, “premeditated”/”instrumental” aggression was reported to be a better predictor of future criminality than “reactive” aggression.
In studies of men who battered their wives, some men’s heart rate rises during marital conflict, and some men’s heart rate lowers. The low-heart-rate group was more likely to have a history of violence outside the marriage, more likely to have a drug dependence, and more likely to have antisocial and aggressive-sadistic characteristics.
Human hunter-gatherers rarely engage in spontaneous “reactive” aggression, while chimpanzees and bonobos engage in conflict three orders of magnitude more often. An unusually high-violence group of Australian aborigines, plagued by poverty and alcoholism, was observed by ethnographers to engage in violence 0.005 times per 100 hours per individual, compared to 1-3 times per 100 hours per individual for chimpanzees and bonobos. In other words, human hunter-gatherers spend at least 1000x less time than apes in violent squabbles with members of their community.
On the other hand, human hunter-gatherers engage in hostile raids and ambushes that are deadlier than anything other primates do. Compared to our nearest primate neighbors, we have extremely low rates of reactive aggression and extremely high rates of proactive (premeditated) aggression.
When animals such as dogs are bred for tameness, it is chiefly defensive aggression that is selected against (since we are selecting primarily for lack of violence against humans, who are neither prey nor conspecifics). Hominid facial morphology has changed in the same way as dog facial morphology, and we have developed a longer developmental period, prolonged play, and cooperative communication, similar to the “domestication syndrome” in other animals.
Some hypothesize that have “bred ourselves” for tameness starting about 200,000 years ago, perhaps through capital punishment of reactively-aggressive, antisocial individuals. Capital punishment appears to be a human universal, and in hunter-gatherer societies it is typically antisocial males with a history of selfish violence who are executed. Capital punishment itself, of course, is an example of proactive aggression – carefully planned and calmly premeditated.
Chimpanzees have a lower death rate from intergroup aggression than human subsistence farmers, but comparable to human subsistence hunter-gatherers, based on 33 human groups from around the world.
Generalizations & Speculations
Defensive aggression is pretty clearly a response to fear and pain, which belongs in the same category with other behaviors like fleeing, hiding, freezing, cowering (protecting vulnerable body parts), and fawning (submission signals.) It is an agitated, reactive, and non-strategic form of aggression, as you can see from the fact that it is relatively ineffective at harming the opponent, and that often an animal in pain will “take its frustration out on” any nearby animals or inanimate objects, regardless of whether they caused the pain. Human experiences like frustration, irritability, or “defensiveness” are probably manifestations of defensive aggression.
Translating social aggression into the human realm is more complicated. It seems clearly related to testosterone, competition, and status conflict, as well as protecting valuable resources (like territory, food, or mates), all of which of course humans do. But it’s unclear to me what the subjective feeling is that corresponds with social aggression. Even valence is unclear – is engaging in social aggression pleasant or unpleasant for animals?
The lateral hypothalamus is generally considered a pleasure center (or at least a “reward-seeking” center), and stimulating it makes rhesus monkeys much more socially aggressive, suggesting that they are in a “seeking”, eager mood when they start fights; the amygdala is associated with fear, and amygdalectomized monkeys are passive and placid and never fight back. So, at least, social aggression is associated with energetic, urgent feelings, but it seems to be a mix or an ambiguous relationship between fear and pleasure-seeking.
Maternal aggression is very clearly associated with fearlessness and the absence of stress. It is a calm, non-agitated, deadly type of aggression. It’s not otherwise clear to me what it “feels like from the inside”, though, or what situations (if any) apart from defending young children it would arise in.
Predatory aggression has a very consistent psychological profile – it’s alert, calm, focused, and eager. It is a strategic and goal-directed kind of aggression, very effective at killing. In humans, it probably shows up during literal hunting (we are a predatory species after all), as well as in strategic types of conflict such as warfare. It seems to have a lot in common with the “flow state” of enjoyable, focused, trance-like absorption in a stimulating activity, which humans also engage in through nonviolent activities such as games and skilled work.
Animal domestication selectively breeds animals for reduced defensive aggression, while preserving other types of aggression (social, maternal, and predatory.) Tame animals are less fearful and skittish around new objects and surprising encounters, less likely to either flee or fight out of fear or irritation.
Human evolution, our own “domestication”, probably did the same thing; we have drastically fewer impulsive, irritable violent reactions to our neighbors than other primates, but probably equal motivation for defending our children and competing for social status, and greater skill than any of our primate relatives in forms of organized violence such as hunting and warfare.
Among contemporary humans, showing frustration is viewed as a sign of weakness, but being calmly dangerous can earn respect. We admire predatory (and social) aggression, but disdain defensive aggression.
As far as hormones go, serotonin seems to clearly correlate with what might be termed “contentment” or “satiety.” It reduces motivation to hunt and to engage in social aggression, reliably across animals. High serotonin levels correlate with and even cause dominant social rank; the very most dominant individuals in a hierarchy are typically less violent, or less severely violent, than the mid-rank individuals, presumably because they’re so high status they don’t have to fight much.
Testosterone seems to increase motivation to engage in both social aggression and social submission, while progesterone inhibits both aggression and submission. This is contrary to the stereotype of submission as “unmanly”.
Perhaps testosterone increases motivation to engage in all social-status-related activities, both fighting and submission, while serotonin has a somewhat independent effect, such that low serotonin increases aggression but not submission.
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