Specification: Neural and hormonal mechanisms in aggression, including the roles of the limbic system, serotonin and testosterone. Genetic factors in aggression, including the MAOA gene.

Limbic system

The biological approach to explaining aggression has three core areas: the neural explanation, the hormonal explanation and the genetic explanation. The main neural explanation is the Papez-Maclean limbic theory involving structures such as the amygdala, hypothalamus, and hippocampus which are implicated in reactive aggression. Reactive aggression is a response to a perceived threat, rather than proactive aggression which is a response in anticipation of a reward. The limbic system also connects to the cingulate gyrus which is responsible for focusing attention on emotionally significant events. Also, the limbic system has connections to the prefrontal cortex which is involved in forward planning and anticipation of reward. The limbic system plays a key role in how an organism responds to environmental threats and challenges and thus is believed to be the key factor in whether we respond aggressively or not to an external stimulus. 

The hypothalamus is responsible for the regulation of the autonomic nervous system, which in turn regulates responses to emotional circumstances. Therefore, damage to this area can result in an inappropriate aggressive response to a perceived threat. The amygdala is responsible for attaching emotional significance to sensory information. The limbic system is believed to be hierarchical with signals being passed from the lower systems to the higher systems in the prefrontal cortex where feelings are monitored and interpreted, which then triggers a physical response. The prefrontal cortex is crucial for regulating social behaviour and aggressive responses. Damage to the prefrontal cortex would reduce the inhibition of the amygdala resulting in higher levels of aggression. 

Neurotransmitters

Under normal circumstances, the neurotransmitter serotonin works on the frontal areas of the brain to inhibit the firing of the amygdala, the part of the limbic system in the brain that controls fear, anger and other emotional responses. Consequently, serotonin has a calming influence and low levels of serotonin mean that people can’t control their impulsive and aggressive behaviour. Serotonin also regulates the pre-frontal cortex; therefore, lower levels of serotonin affect our response to external stimuli, meaning the person becomes aggressive easily and can’t control their responses in a ‘normal’ way. They can’t anticipate risk and therefore impulsively engage in aggressive behaviour. 

Hormones

Observations of non-human and human species have demonstrated that aggression is more evident in males than in females. Animal studies have led to the explanation that male hormones are implicated in aggression. The main hormone which decides whether an embryo develops into a male or female is testosterone. Testosterone peaks in young adolescent males before gradually declining with age. It also promotes muscle strength and is responsible for the sex drive. However, testosterone is also implicated in aggression. 

Evaluation

Kluver and Bucy (1939) were early researchers who, using Rhesus monkeys, removed the main areas of the limbic system including the amygdala, hippocampus and surrounding cortical areas. They found that the monkeys displayed an absence of emotional, motor and vocal reactions normally associated with stimuli or situations eliciting fear and anger. Lesioned monkeys also lost the social understanding of group hierarchies and would try to fight the more dominant and larger members of the group. This research demonstrates the importance of the limbic system in regulating aggressive responses. One of the main criticisms of research using animals to provide evidence for aggression in humans is the differences between animal and human physiology and the question of whether we can extrapolate research findings from animals to human aggressive behaviour. Despite humans and monkeys both possessing similar neural structures, we cannot be sure that the processes involved in mediating aggression in humans are the same as those shown in animals such as the Rhesus monkey. 

More recent technological advances have allowed neuroimaging techniques such as MRI scans to investigate the relationship between neural structures such as the amygdala and aggressive behaviour. Wong et al. (1997) undertook MRI scans of 19 violent male criminals in Broadmoor hospital and compared the size of the amygdala with 20 ‘normal’ control subjects. He found that the volume of the amygdala was significantly smaller in the 19 violent criminals, thus supporting the role of the amygdala and limbic system in aggression. One of the problems with this research is a lack of population validity: the sample was relatively small, and thus the issue of whether these findings can be generalised to the wider population can be raised. The research can be accused of gender bias, as their research was confined to males; therefore, caution must be taken in using this research to explain aggression in females. When research is used to explain behaviour is both males and females yet only undertaken on males, this is called beta bias. 

Ferrari et al. (2003) provide support for the role of serotonin in aggressive behaviour. They allowed adult male rats to fight with another rat at a specific time for ten days. On the eleventh day, the rat wasn’t allowed to fight. However, researchers found that the rat’s dopamine levels had raised by 65%, and his serotonin levels were reduced by 35%. Despite the fact that the rat was not fighting, the experience had changed the rat’s brain chemistry. Ferrari et al.’s (2003) research raisesthe question of whether lower levels of serotonin cause aggression or whether they are a response to aggression being carried out. The issue of cause and effect is a key factor in the explanation of aggressive behaviour. The aim of any science is to establish the cause by measuring the effect. However, if the cause, i.e. lower levels of aggression, are the effect, this substantially lowers the validity of the explanation as to the causes of aggression. Nevertheless, this research does demonstrate the complexity of the role of serotonin in aggressive behaviour. 

Mann et al. (1990) administered the drug dexfenfluramine (which depletes serotonin in the brain) to 35 healthy adults. The researchers then used a questionnaire to assess hostility and aggression levels, which rose following administration of dexfenfluramine amongst males, but interestingly not amongst females. The research by Mann et al. (1990) demonstrates the issue of beta bias that is inherent in neural explanations of aggression and shows that males and females may not be subject to the same physiological factors when explaining aggression. 

Psychologists interested in finding out if testosterone was implicated in aggression decided to test out this theory by castrating animals, thereby removing their testes. Wagner (1979) castrated mice and aggression levels went down, thus providing support to the theory that testosterone is implicated in aggression. Wagner’s (1979) research however only provides correlational support for the cause of aggression, as the research only demonstrates a relationship between lowered testosterone and lowered aggression. However, Wagner’s (1979) research does demonstrate that testosterone plays a crucial role in aggressive responses. 

Possible Exam Questions 

1. Outline and evaluate the role of neural and/or hormonal mechanisms in aggression. (16 marks) 

2. Micah was experiencing outbursts of temper at home and school. His friends and family were concerned that he seemed to have no control over his temper. Micah has two older sisters, and they are both doing very well in school and are calm and easy going. Micah’s grandfather had spent some time in prison for arson and Micah’s father had died when Micah was younger in a fight. Using your knowledge of the genetic, neural and hormonal mechanisms in aggression explain why Micah may be having trouble controlling his temper. (12 marks)