4.3.8 Aggression Flashcards
1
Q
neural mechanisms in aggression
A
- mechanisms of the nervous system, including the limbic system of the brain and the neurotransmitter serotonin
2
Q
the limbic system
A
- an area of the brain associated with the regulation of emotions
- the amygdala in particular is associated with aggression;
- Gospic et al. (2011) used fMRI brain scans to measure brain activity during a game designed to provoke aggression, and found that aggressive responses were correlated with increased activity in the amygdala
- also, patients who were given drugs that reduced amygdala activity were less aggressive
3
Q
the role of serotonin
A
- an inhibitory neurotransmitter associated with the regulation of impulsive behaviour
- low levels are thought to increase aggression, as it reduces self-control and leads to an increase in impulsive behaviour
- high levels are thought to decrease aggression;
- Berman et al. (2009) conducted an experiment where he gave half the ppts paroxetine (an SSRI that increases serotonin levels) and the other half a placebo
- the paroxetine group consistently gave fewer and less intense electric shocks than the placebo group
- this supports the link between serotonin and aggression
4
Q
neural mechanisms in aggression - strengths
A
- brain scans of convicted murderers by Raine et al. (1997) found abnormalities in the amygdala and other areas of the limbic system compared to controls, supporting the link between this and aggression
- Virkkunen et al. (1994) found that impulsive violent offenders in prisons had lower serotonin levels compared to controls, supporting the link between this and aggression
5
Q
neural mechanisms in aggression - limitations
A
- neural explanations are deterministic, as it implies people aren’t morally responsible for aggressive behaviour, as it’s not freely chosen
- it may be a correlation rather than causation, e.g. as there are aggressive people with normal limbic systems OR e.g. serotonin could decrease in response to angry feelings, so it’s an effect of aggression rather than a cause
- questions of external validity, as Berman et al. based their conclusions on games played in lab conditions, which may not reflect behaviours in real life
- conflicting evidence, as Huber et al. (1997) injected crayfish with serotonin and it made them behave more aggressively rather than less (although as an animal study, these findings may not be valid when applied to humans)
6
Q
hormonal mechanisms in aggression
A
- testosterone is the primary sex hormone in males and is linked with aggression
- several studies have found that high testosterone is correlated with increased aggression;
- Dabbs et al. (1995) found that prisoners who’d committed violent crimes had higher testosterone levels than those who were convicted of non-violent crimes
- Van Goozen et al. (1995) found that administering testosterone to female-male transgenders resulted in more aggressive behaviour, and male-females who were given drugs to lower testosterone levels behaved less aggressively
7
Q
hormonal mechanisms in aggression - strengths
A
- research support from both studies above
- evidence of this in animals too, e.g. Albert et al. (1989) found that injecting female rats with testosterone made them behave more aggressively
8
Q
hormonal mechanisms in aggression - limitations
A
- Dabbs et al. only shows that high testosterone levels are correlated with aggression, not that it causes aggression
- conflicting evidence, as Tricker et al. (1996) randomly assigned 43 men to receive either 600mg of testosterone per week or a placebo, and he found no difference in aggression between the two groups
- deterministic as it implies people aren’t morally responsible for their behaviour as it’s not freely chosen
9
Q
genetic factors in aggression
A
- ties in with other biological factors, i.e. a person may have genetics that predispose them to limbic system abnormalities or low serotonin activity
- twin studies are useful in determining the genetic basis of aggression, because if concordance rates are higher in MZ twins than DZ twins, it shows that genetics plays a role;
- Coccaro et al. analysed data from 182 pairs of MZ twins and 118 pairs of DZ twins, and the concordance rate for physical violence was 50% among MZ and 19% among DZ twins
- Christiansen (1977) analysed concordance rates for criminal convictions among 3586 pairs of twins, and found they were higher for MZ twins than DZ twins in both males and females
- this suggests there’s a genetic component to aggression
10
Q
the MAOA gene
A
- a gene that’s particularly associated with aggression
- responsible for production of MAOA which is an enzyme that breaks down serotonin within the synaptic cleft after neurotransmission
- the low-activity form of the gene is known as the MAOA-L / ‘warrior gene’ as it results in lower serotonin being broken down, so a higher rate bonds to receptors on the post-synaptic neuron, which decreases self-control and increases impulsive behaviours like aggression
- discovered by Brunner et al. (1993) who studied a large Dutch family who were all actively engaged in aggressive behaviours and crime, and found that they all had unusually low MAOA levels
11
Q
genetic factors in aggression - strengths
A
- many other studies support this link, e.g. McDermott et al. (2009) found that ppts with the MAOA-L gene punished people more aggressively than subjects without the MAOA-L gene in a game situation
- research support for correlations of the MAOA gene and aggression in both directions, as Mertins et al. (2011) found that ppts with high MAOA activity levels behaved more compassionately in a monkey-lending game
12
Q
genetic factors in aggression - limitations
A
- there are exceptions as many people with the MAOA-L gene aren’t overly aggressive, and many aggressive people don’t have this gene
- other factors must affect aggression, because if it was entirely due to genetics, then concordance rates would be 100% for MZ twins, but they were only around 50%
- an interactionist approach, using the diathesis-stress model, may be better as many studies have shown that environmental factors interact with the MAOA-L gene to increase the likelihood of aggression, e.g. Frazzetto et al. (2007) found that low MAOA levels only resulted in higher aggression when accompanied by traumatic childhood events which had occurred in the first 15 years of life
- deterministic as it suggests people aren’t morally responsible for aggressive behaviour as they aren’t in control of it
- McDermott et al’s study isn’t representative of a real-life situation, so results can’t be generalisable
13
Q
ethological explanations of aggression
A
- studies aggression in animals to provide insights into aggression in humans
- sees aggression as an adaptive trait, because it;
- promotes their survival; ‘losers’ will seek out new territory elsewhere, leaving more room and resources for the species which enhances their survivability
- increases their social status within a hierarchy; many animal species involve displays of aggression for them to climb the hierarchy and present themselves as more attractive
14
Q
ritualistic aggression
A
- aggression within animal species is often ritualistic, because very little physical damage takes place in fights between animals of the same species (or else they could die and go extinct)
- rituals enable members of a species to compete and establish dominance without harming each other, as the ‘loser’ will make themselves vulnerable to the victor, e.g. wolves displaying their neck to signal defeat
15
Q
innate releasing mechanisms
A
- biologically hard-wired mechanisms for aggression, e.g. brain structures or neural pathways
- environmental cues trigger the innate releasing mechanism which releases a fixed action pattern of behaviour
- e.g. male sticklebacks have an innate releasing mechanism that activates a fixed action pattern at the sight of a red spot, with the evolutionary purpose of fighting off male competition using aggression
16
Q
fixed action patterns
A
- a set sequence of behaviour that occurs automatically due to an innate releasing mechanism
- they have several key features;
- fixed; relatively unchanging and unaffected by learning
- universal; found in every individual of the species
- ballistic; once initiated, it can’t be stopped and the animal will keep going until the behaviour is complete
- single-purpose; only occurs for one reason
- e.g. during mating season, male sticklebacks build nests where females lay eggs. males develop red bellies during this time, and if another male enters their territory, the stickleback will attack it
17
Q
ethological explanations of aggression - strengths
A
- Tinbergen (1952) demonstrates how fixed action patterns in sticklebacks are universal and innate, as he presented them with models of fish with red bellies and they all responded with the same fixed action pattern of fighting behaviour (even when the model was unrealistic looking)
- many examples of fixed action patterns beyond this as well, e.g. if an egg is placed near a Grelag goose, it’ll instinctively try to roll the egg into its nest in a fixed action pattern
- evidence from previous explanations, e.g. the MAOA gene explanation corresponds with the ethological one as it also suggests an innate basis for aggression
18
Q
ethological explanations of aggression - limitations
A
- animals like sticklebacks are very different to humans, so there are questions of validity in humans as these explanations of aggression may not apply
- human aggression is also very different to animal aggression, e.g. humans have wars and weapons like guns, which animals don’t
- conflicting evidence as Schleidt (1974) argues that fixed action patterns are often quite varied, so some ethologists prefer the term modal action pattern