Discuss the neurobiological circuitry and empirical evidence that supports the
idea that aggression is rewarding
Aggression is defined as “any behaviour that harms another individual who is
motivated to avoid such harm” (Benjamin Jr, 2015). Humans generally look down
upon aggressive behaviour as it is viewed as impulsive, antisocial and posing
negative consequences to both “victims… and perpetrators” (Bresin, 2019).
However, in evolutionary history and among many different species today,
aggression is itself “a biological mechanism shaped by natural selection into an
adaptive force which helps to establish and maintain primate societies” (Bernstein,
1974), perhaps by attracting mates and protecting other group members from threat.
In the absence of these evolutionary driving forces, there remains the question as to
why animals often resort to aggression even when this behaviour is unnecessary.
Recent studies have indicated that aggression is itself a motivational factor, as it has
been found to be linked with activation of the reward circuit in the brain. Emerging
evidence from recent animal and human studies shows a connection between
aggressive behaviour and activation of the reward circuit in the brain; but, in humans,
more evidence is needed to determine a causal role.
Animal studies involving mice have often used operant conditioning as a tool for
investigating the rewarding effects of aggression, finding a strong link between this
behaviour and activation of the reward circuit, including the Nucleus Accumbens and
dopamine receptors. Operant conditioning is the study of reversible behaviour
maintained by reinforcement (Staddon, 2003), first demonstrated by Skinner in his
classic lever-pressing experiments (Pritchett, 2004). This experimental method has
since been implemented for the study of the neural mechanisms involved in
aggression and reward. Couppis and Kennedy (2008) developed a study in which
resident mice were trained to nose-poke on a VR-5 reinforcement schedule in order
to earn access to an intruder mouse, to then be injected with varying levels of D1and D2-like receptor antagonists (Couppis, 2008). They found that 50-ng SCH23390 suppressed aggressive response rates by 40%, while 25 and 50 ng sulpiride
doses almost completely inhibited responding and suppressed biting by 50%
(Couppis, 2008). Their results indicate that dopamine receptors are involved in
whether or not mice experience aggression as rewarding, as the more the dopamine
response is inhibited, the less the mice respond aggressively. Further research is
needed as a causal role between aggression and reward cannot be inferred from
these results. Golden et al. (2019) developed a mouse model of appetitive operant
aggression, using immunohistochemistry and in situ hybridization to measure Fos
(Golden S. A., 2019). The Fos protein product is often used as an indicator of
neuronal activity in the NAc, part of the reward system in the brain. They found that
“the inhibition of NAc Drd1- but not Drd2-expressing neurons decreased aggression
self-administration and seeking” (Golden S. A., 2019), supporting Couppis’ earlier
findings of a link between dopamine and the rewarding components of aggression.
Golden et al. (2019) were also able to establish a causal role of dopamine, as they
used a transgenic hybrid breeding strategy to breed mice with inhibited NAc Drd1and Drd2-expressing neuron activity, finding that “30-50% of the F1 hybrids do not
acquire operant aggression self-administration” (Golden S. A., 2019). This is a
particular strength of the study as it shows that aggressive behaviour is only
exhibited on a repetitive basis when there is excitation of the dopamine receptors in
the reward circuit of the brain.
Classical conditioning is also a commonly used experimental method for the study of
aggression and reward in mice, often referred to as conditioned place preference
(CPP). CPP is “a form of Pavlovian conditioning routinely used to measure the
rewarding or aversive motivational effects of objects or experiences” (Cunningham,
2006). In the case of neurobiological research on aggression and reward, the
motivational experience is aggression itself. Golden et al. (2016) established a
mouse model to measure the valence of aggressive social interaction between a
resident mouse and smaller subordinate intruder, as reinforcement for the
development of CPP (Golden S. H., 2016). They found that the aggressor mice
developed a ”behavioural preference for environmental contexts associated with the
interaction” (Golden S. H., 2016), suggesting that a CPP was indeed exhibited by the
mice. CPP experiments have typically been used to study the rewarding effect of
drugs, as mice tend to return to the environment in which they experienced the
pleasant or rewarding sensation. In CPP studies of aggression, we may assume the
same behavioural motivation – mice return to the environment in which they
experienced pleasure or reward through aggressive interactions. They also found a
“critical GABAergic projection from the BF to the LHb that bidirectionally controls
aggression motivation” (Golden S. A., 2019). Since the lateral habenula has been
found to be “a major candidate for a source of negative reward-related signal in
dopamine receptors” (Matsumoto, 2007), it can be concluded that aggression during
CPP activated the reward circuitry of the brain. However, further research in this area
is needed “to cover the full spectrum of ethologically relevant aggressive behaviors”
(Golden S. A., 2019), such as unconditioned as well as conditioned aggression, so
that there is a deeper understanding of the neural mechanisms involved in
aggression-reward. Furthermore, a typical limitation of the studies involving
aggression and reward (including Golden’s study) is that they often conduct their
research with only male rats – leaving others to question whether this same
behaviour is exhibited in female rats also. Börcher’s (2023) study aimed to
investigate this by conducting an experiment in which both male and female rats
underwent aggression CPP training, while being measured for mesolimbic dopamine
turnover. They found that female rats “experience winning aggressive behaviors as
rewarding, and do so to a similar extent as male rats in a dopamine-dependent
manner” (Borchers, 2023). This suggests that there is a similar neural circuitry
between both male and female rats in regards to aggression and reward; although,
further research in this area is needed to establish the extent of any differences that
may be present as there is the question that female rats and mice “differ in how
rewarding they perceive aggression or how much they are willing to act on it”
(Borchers, 2023).
Mice and rat studies have allowed for researchers to examine brain circuitry post
mortem, as well as other experimental techniques that would be unethical to conduct
on humans. However, as much information as can be gained from these studies, the
results cannot be generalised to humans. Human studies into aggression and reward
have found a link between the two, but in much weaker terms. Ramírez et al (2006)
conducted a self-report study in which participants were asked questions relating to
hedonicity, decision making, justification of aggression and impulsiveness. They
found that “mean hedonicity ratings followed a bell curve with increasing levels of
aggressiveness” with participants choosing “neither passive nor highly aggressive
responses to social conflicts” (Ramirez, 2006). As Ramírez concluded, this suggests
that individuals experience aggression as pleasant and rewarding up to a certain
point, as responses of medium intensity were rated as less unpleasant than the most
passive or most aggressive responses (Ramirez, 2006). The self-report nature does
present some limitations for the validity of the study, as participants may have felt
reluctant to admit to finding more aggressive responses as pleasant, so as to
present themselves in a more appealing manner. Ramírez’s study also did not
consider the neural mechanisms playing a part in whether or not aggression was
deemed as rewarding. Chester et al (2015) did consider the neurobiological circuitry
at play during aggression and reward-seeking, and found that “lower-functioning
DRD2 profiles were associated with greater sensation-seeking, which then predicted
greater aggression”, putting these individuals “at risk for violence because it
motivates them to experience aggression’s hedonically rewarding qualities” (Chester,
2015). This provides support for previous mouse studies that have found dopamine
to be an important factor in whether mice experience aggression as rewarding, as
here it can be seen that individuals with reduced dopaminergic brain activity find
themselves seeking reward through aggression and violence. As is a problem with
most human studies, it can only be inferred that there is a link or correlation between
aggression and reward; thus, causation cannot be determined. Furthermore, the
study involved only students of Caucasian heritage meaning that results cannot be
applied across cultures – perhaps there is a need for further research into the
cultural differences of whether aggression is experienced as pleasurable.
Aggression is likely a highly rewarding experience for most animals. In mice,
aggression has consistently been seen to activate the reward circuitry of the brain,
as inhibition of specific dopamine receptors significantly reduced aggressive
responding. Dopamine has also been linked with human experiences of aggression,
as individuals lower in dopaminergic brain activity often resort to violence for the
‘high’ that it provides. What remains clear is that humans and animals experience the
rewarding effects of aggression at varying degrees and intensity, and more research
is needed to determine whether this is due to social factors and norms present within
humans and not animals, or whether there are significant differences in brain
functioning between the two.
References
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