aggression Flashcards
hot blooded aggression with example and definition
angry and impulsive behaviour couple with physiological arousal
Eg. Tony martin (1999): shot at 3 intruders, killed 1 (a 16 year old) following a spate of burglaries at his home. Initially sentenced to life imprisonment; commuted to 3 years due diminished responsibility.
cold blooded aggression def and example
premeditated way of getting what you want eg. Rape, murder.
Case: the moors murders: Ian Brady and Myra Hindley (1963-65): killed 5 children and buried the bodies in saddleworth moors.
What are the brain regions associated with the limbic system?
Amygdala
Thalamus/ Hypothalamus
Hippocampus
What is a key role of the limbic circuit?
Collection of structures in the centre of the brain.
In humans and animals, the amygdala acts as a threat sensor from the environment. in humans there is a positive correlation between how reactive the amygdala is and aggression levels in a n individual.
What is the limbic circuit also known as?
Papez cuircit
What are three key regions of the limbic system involved in aggression?
The limbic system is a collection of structures in the centre of the brain. One of its functions is to processes emotional responses such as aggression.
The amygdala has been identified as being linked to the production of aggressive behaviour, FMRI’s show increased activity during aggressive responses. (Gospic)
The hypothalamus has a role in integrating and expressing emotional responses, it can trigger aggressive behaviour as part of the fight or flight response.
These areas of the limbic system communicate with an external layer of the brain, the OFC, controls executive function (decision making) which attempts to control aggression produced by the limbic system.
What is the link between Kluver & Bucy’s (1937) research in animals and Kluver-Bucy syndrome
Discovered the destruction of the amygdala in a monkey who was dominant in a social group caused it to lose its dominance in the group.
Kluver-Bucy syndrome is a rare neuropsychiatric disorder due to lesions affecting bilateral temporal lobes, especially the hippocampus and amygdala; symptoms include placidity.
What did Mark & Ervin (1970) report in a patient receiving stimulation to her amgydala?
A woman receiving painless stimulation to her amygdala became enraged and smashed her guitar against the wall.
Explain the research by Gospic et al. (2011), and how it sheds light on the role of the limbic system in aggression.
In this research ppts played ‘the ultimatum game’. Subject a is termed the proposer, subject B is the responder. Subject B was subjected to mild provocation.
The researchers used fMRI to monitor brain activity while playing.
They found that when subject B rejected the offer there was increased response in the amygdala in those subjects.
They also found that when the ppts took Benzodiazepines, which are used to calm anxiety, it halved the number of rejections and decreased amygdala activity.
In conclusion it suggests an association between reactive aggression and the amygdala.
LIN et al. (2011) - research for neural mechanisms of aggression
Ontogenetic: by introducing light sensitive proteins into target cells, researchers can precisely activate or inhibit these cells with light pulses.
Line et al:
They used optogenetics to stimulate the hypothalamus to investigate its role in controlling aggression in male mice.
Activation of this area caused aggressive behaviours, such as attacking other mice and even inanimate objects.
Inhibition of the hypothalamus caused the mices aggressive behaviours to subside
This research provided direct evidence that the hypothalamus (which received connections from the amygdala) is a critical brain region for initiating and regulating aggression.
What evidence is there for a role of serotonin in violent behaviour?
Serotonin has widespread inhibitory effects on the brain – slowing down neuronal activity.
Aggression in humans and animals is associated with low levels of serotonin.
Normal levels in the OFC reduce the firing of neurons and allow for a greater degree of behavioural self control.
Decreased levels disturb this mechanism reducing self control and increasing impulse behaviour (including aggression).
animal studies for neural mechanisms of aggression
Pharmacologically blocking or genetically modifying 5-HT2a receptors. Mice with a deletion of the gene responsible for 5-HT2a expression exhibit less aggressive behaviour compared to typical mice. Stimulating 5-HT2a can lead to aggression, especially when the animal perceives threat or competition.
antipsychotics for neural mechanisms for aggression
Drugs for schizophrenia block the D2 receptor, but some have impacts on other receptors. Risperidone and olanzapine block the 5-HT2a receptor, and have been shown to reduce aggression in patients with schizophrenia or dementia.
serotonergic metabolites for neural mechanisms for aggression
Viekunnen et al (1994)
Viekunnen et al (1994) compared levels of a serotonin breakdown product (5-HIAA) in the cerebrospinal fluid of violent impulsive and violent non-impulsive offenders. The levels were significantly lower in the impulsive offenders. The levels were significantly lower in the impulsive offenders. This is because the reduction of the 5-H1AA means that there is decreased serotonin activity in the brain which has an effect on controlling impulsive (reactive) aggressive behaviour.
serotonin-depletion studies for neural mechanisms for aggression
Passomonti et al. (2012) used acute tryptophan depletion (ATD) as a way to temporarily reduce serotonin (tryptophan is the precursor for serotonin). The results showed that ATD reduced connectivity between the PFC and amygdala when participants viewed angry faces, suggesting that oownserotonin might impair the PFCs ability to regulate the amygdala’s response to aggression-related cues.
post morgen studies for neural mechanisms for aggression
Rosell and Siever (2015) reviewed post-mortem studies indicating that individuals with histories of impulsive aggression or violent behaviour often show an up regulation of 5-HT2a receptors (perhaps compensating for low serotonin) in the PFC, particularly in the orbitofrontal cortex.
Neural mechanisms for aggression AO3
A strength of the argument supporting the involvement of limbic activity n in aggression, comes from studies in offenders suggesting that abnormal activity in brain areas associated with emotion regulation may play a role in violent behavior.
E – Raine et al (1997) used PET scans to compare the limbic activity of individuals who had committed murder by reason of insanity with non-murderers, finding reduced activity in limbic regions in the murderer group.
E – additionally, asymmetries in the limbic activity (L<R), we’re found, which could impair emotional processing and regulation.
C – however, murder due to insanity may not be directly equate to directly aggression. A study by Coccaro et al. (2007) therefore provides important context, showing that patients with Intermittent Explosive Disorder (IED) exhibited reduced activity in the OFC and amygdala when shown angry faces.
L – the reliabaility of these findings is strengthened by the use of PET scanning in both studies, which provides objective and consistent measurements of brain activity, supporting the interpretation that dysfunction in limbic and prefrontal regions may contribute to aggression.
neural mechanism for aggression AO3
A strength of the argument that the limbic system is involved in aggression comes from case study evidence that damage to the limbic system through trauma or disease can lead to aggressive behaviors.
E – Burns and Swerdlow (2003) reported a case study which pedophelia emerged following a tumor in the orbitofrontal cortex, which resolved after surgery.
E – this demonstrates that disruption of the amygdala can lead to aggression and is supported by a similar case study reported by Sumer (2007) of a 14 year old girl with extreme aggression was shown to be result of a tumor pressing on her amygdala
C – although these findings are supportive, it must be acknowledged that case studies may not allow extrapolation to the population; it would be important to know which efferent and afferent connections to the amygdala in these cases were implicated, for example.
L – taken together, these findings demonstrate that case study evidence is consistent with other data, such as functional imaging studies, indicating that limbic activity relates to aggressive behaviour, though the case study data should be interpreted with caution and triangulated with other evidence.
neural mechanisms for aggression AO3
A strength of the serotonin explanation for aggression comes from drugs research, which shows that increasing serotonin activity reduces aggressive behavior.
E – Berman (2009) conducted a study in which ppts were given either a placebo or a does of paroxetine (a drug that increases serotonin activity). Ppts then took part in a lab based game were they administered shocks in response to provocation. The findings revealed that ppts who received paroxetine consistently gave fewer and less intense shocks, particularly among those with a prior history of aggressive behaviour.
E – the demonstrates that an increase in serotonin reduces aggression in a controlled experimental setting, offering evidence beyond correlational findings commonly reported in serotonin studies.
C – however, while these results are promising, the interpretation is limited by the lack of direct measures of serotonergic activity such as receptor occupancy or serotonin levels in the brain. Without these measures, it is unclear whether the observed reduction in aggression is directly due to increased serotonergic transmission or other indirect effects of paroxetine.
L – overall, the findings, though suggestive, do not conclusively establish a causal link between serotonin activity and aggression, which undermines their validity. To more robustly support the serotonin hypothesis, future studies should incorporate neuron marine or biochemical essay as to directly measure changes in serotonin receptor activity in response to drug administration.
neural mechanisms for aggression AO3
A limitation of research on the neural basis of aggression is that much of it is correlational, which restricts our ability to establish causality.
E – correlational studies are often necessary due to ethical constraints, as directly provoking aggression in a laboratory setting would not protect ppts from harm. As a result researchers frequently rely on brain scans to observe correlations between aggression and brain structures like the amygdala or orbitofrontal cortex (OFC).
E – however, without experimental manipulation, it remains uncertain whether changes in the amygdala or OFC lead to increased aggression, or if aggressive behaviour might induce changes in these brain regions.
L – this limitation raises the possibility of an unidentified third variable influencing both aggression and neural changes, such as fluctuate level of neurotransmitters. Consequently, while these studies provide valuable insights, their correlational nature limits the validity conclusions we can draw about causation in aggression research.
