outline research into institutional aggression

AQA Psychology A Unit 3

This website gives model answers to all potential 24 mark questions in the topics of relationships, aggression and gender in unit 3 of AQA Psychology A. This blog is relevant to the current specification (as of 2015). Use the tools on the right to view answers by topic or by past paper. Click each question to see the full answer. Happy revising!

Outline research into institutional aggression. (4 marks)

2 comments :.

did you get full marks for this answer?

I did a similar answer and got full marks but my teacher said maybe add a few names of researchers, so Irwin and Cressey for the importation model

Institutional Aggression: Prisons

Dispositional explanation of aggression.

Institutional aggression refers to an aggressive or violent behaviour that takes place within the social context of a formal organised setting. It can be explained in terms of disposition or situation.

Disposition or situation

• One dispositional explanation is known as the importation model.
• Situational explanations identify causes of behaviour that exist within the environment.

The importation model

• Developed by Irwin and Cressey (1962) , the importation model is the most influential dispositional explanation of how aggression develops within prisons.
• This includes beliefs, values, norms, attitudes, and a history of learning experiences, as well as other personal characteristics such as gender, race and class.

The convict subculture

• The willingness of inmates to use violence inside prison to settle disputes reflects their lives before they were imprisoned.
• Inmates, therefore, import behaviours as a means of negotiating their way through the unfamiliar and frightening prison environment.
• In this environment, existing inmates use aggression to establish power, status, influence and access to resources; in other words, the convict subculture.

Predisposed aggression

• Aggression is therefore the product of individual characteristics of inmates and not of the prison environment.
• Inmates predisposed to using violence would be likely to do so in any setting.

Delisi et al. (2011)

• Delisi et al. (2011) studied 813 juvenile delinquents confined in Californian institutions.
• Experiences of childhood trauma, high levels of anger and irritability, a history of substance abuse, and a history of violent behaviour.

Delisi et al. (2011) findings

• These inmates were more likely to engage in suicidal activity and sexual misconduct, and committed more acts of physical violence when compared to a control group of inmates with fewer negative dispositional factors.

Situational Explanation of Aggression

Situational explanations

• In contrast to dispositional factors, situational explanations identify the causes of behaviour as existing within the environment, which may include other people.

The deprivation model

• Clemmer (1958) developed the deprivation model.
• This places the causes of institutional aggression within the prison environment itself.
• According to Clemmer , harsh prison conditions are stressful for inmates, who have to cope by resorting to aggression and often violent behaviour.

Prison conditions

• These conditions include being deprived of freedom, independence, goods and services, safety, and heterosexual intimacy.
• Deprivation of material goods is especially important because it increases competition amongst inmates to acquire them, which is often accompanied by a corresponding increase in aggression.

Prison regime

• Aggression is also influenced by the nature of the prison regime.
• Prison regimes can be unpredictable and regularly use ‘lock-ups’ to control behaviour.
• This creates frustration, reduces stimulation by barring other more interesting activities, and reduces access to goods even further.
• This is a recipe for violence, which becomes an adaptive solution to the problem of deprivation.

Steiner (2009)

• Steiner (2009) investigated factors that predicted inmate aggression in 512 US prisons.
• In this study, the factors reliably predicted aggression in line with the deprivation model.

Steiner (2009) results

• Female staff,
• Black inmates,
• Hispanic inmates,
• Inmates in protective custody for their own safety.
• These represent prison level factors because they are independent of the individual characteristics of inmates.
• This supports the deprivation model.

Studies on Dispositional & Situational Aggression

Harer and Steffensmeier (1996) investigated the dispositional explanation of violence in prisons. Magargee (1977) investigated the effect of overcrowding (population density) in prisons and violent behaviour.

Harer and Steffensmeier method

• Case study.
• Data was examined from 58 male prisons in the US. They looked for racial differences in violence and drug/alcohol misuse.

Harer and Steffensmeier results

• Black males were more likely to be involved in violent incidents, whilst white males were more likely to be involved in drug/alcohol misuse.
• Supports the importation model which suggests inmates ‘import’ their outside of prison behaviour into prison. Also supports the dispositional explanation of aggression that suggests that aggressive behaviour is a character trait and not a result of the situation.

Harer and Steffensmeier evaluation

• Ecological validity.
• Large sample.
• Racism – cultural bias.
• Ignores socioeconomic factors outside of prison.

Magargee (1977) method

• A correlation.
• A prison for male young offenders was studied for 3 years. The population density and number of violent incidents were correlated.

Magargee (1977) results

• A positive correlation was discovered. The more overcrowded the prison was, the more incidents of violence were recorded.
• Chronic overcrowding, which is common in many prisons, increases violence. Suggesting situational factors have a large influence on aggression.

Evaluation of Magargee (1977)

• Practical applications.
• Correlations cannot show cause.
• Individual, cultural and social variations.

1 Social Influence

1.1 Social Influence

1.1.1 Conformity

1.1.2 Asch (1951)

1.1.3 Sherif (1935)

1.1.4 Conformity to Social Roles

1.1.5 BBC Prison Study

1.1.6 End of Topic Test - Conformity

1.1.7 Obedience

1.1.8 Analysing Milgram's Experiment

1.1.9 Agentic State & Legitimate Authority

1.1.10 Variables of Obedience

1.1.11 Resistance to Social Influence

1.1.12 Minority Influence & Social Change

1.1.13 Minority Influence & Social Impact Theory

1.1.14 End of Topic Test - Social Influences

1.1.15 Exam-Style Question - Conformity

1.1.16 Top Grade AO2/AO3 - Social Influence

2.1.1 Multi-Store Model of Memory

2.1.2 Short-Term vs Long-Term Memory

2.1.3 Long-Term Memory

2.1.4 Support for the Multi-Store Model of Memory

2.1.5 Duration Studies

2.1.6 Capacity Studies

2.1.7 Coding Studies

2.1.8 The Working Memory Model

2.1.9 The Working Memory Model 2

2.1.10 Support for the Working Memory Model

2.1.11 Explanations for Forgetting

2.1.12 Studies on Interference

2.1.13 Cue-Dependent Forgetting

2.1.14 Eye Witness Testimony - Loftus & Palmer

2.1.15 Eye Witness Testimony Loftus

2.1.16 Eyewitness Testimony - Post-Event Discussion

2.1.17 Eyewitness Testimony - Age & Misleading Questions

2.1.18 Cognitive Interview

2.1.19 Cognitive Interview - Geiselman & Fisher

2.1.20 End of Topic Test - Memory

2.1.21 Exam-Style Question - Memory

2.1.22 A-A* (AO3/4) - Memory

3 Attachment

3.1 Attachment

3.1.1 Caregiver-Infant Interaction

3.1.2 Condon & Sander (1974)

3.1.3 Schaffer & Emerson (1964)

3.1.4 Multiple Attachments

3.1.5 Studies on the Role of the Father

3.1.6 Animal Studies of Attachment

3.1.7 Explanations of Attachment

3.1.8 Attachment Types - Strange Situation

3.1.9 Cultural Differences in Attachment

3.1.10 Disruption of Attachment

3.1.11 Disruption of Attachment - Privation

3.1.12 Overcoming the Effects of Disruption

3.1.13 The Effects of Institutionalisation

3.1.14 Early Attachment

3.1.15 Critical Period of Attachment

3.1.16 End of Topic Test - Attachment

3.1.17 Exam-Style Question - Attachment

3.1.18 Top Grade AO2/AO3 - Attachment

4 Psychopathology

4.1 Psychopathology

4.1.1 Definitions of Abnormality

4.1.2 Definitions of Abnormality 2

4.1.3 Phobias, Depression & OCD

4.1.4 Phobias: Behavioural Approach

4.1.5 Evaluation of Behavioural Explanations of Phobias

4.1.6 Depression: Cognitive Approach

4.1.7 OCD: Biological Approach

4.1.8 Evidence for the Biological Approach

4.1.9 End of Topic Test - Psychopathy

4.1.10 Exam-Style Question - Phobias

4.1.11 Top Grade AO2/AO3 - Psychopathology

5 Approaches in Psychology

5.1 Approaches in Psychology

5.1.1 Psychology as a Science

5.1.2 Origins of Psychology

5.1.3 Reductionism & Problems with Introspection

5.1.4 The Behaviourist Approach - Classical Conditioning

5.1.5 Pavlov's Experiment

5.1.6 Little Albert Study

5.1.7 The Behaviourist Approach - Operant Conditioning

5.1.8 Social Learning Theory

5.1.9 The Cognitive Approach 1

5.1.10 The Cognitive Approach 2

5.1.11 The Biological Approach

5.1.12 Gottesman (1991) - Twin Studies

5.1.13 Brain Scanning

5.1.14 Structure of Personality & Little Hans

5.1.15 The Psychodynamic Approach (A2 only)

5.1.16 Humanistic Psychology (A2 only)

5.1.17 Aronoff (1957) (A2 Only)

5.1.18 Rogers' Client-Centred Therapy (A2 only)

5.1.19 End of Topic Test - Approaches in Psychology

5.1.20 Exam-Style Question - Approaches in Psychology

5.2 Comparison of Approaches (A2 only)

5.2.1 Psychodynamic Approach

5.2.2 Cognitive Approach

5.2.3 Biological Approach

5.2.4 Behavioural Approach

5.2.5 End of Topic Test - Comparison of Approaches

6 Biopsychology

6.1 Biopsychology

6.1.1 Nervous System Divisions

6.1.2 Neuron Structure & Function

6.1.3 Neurotransmitters

6.1.4 Endocrine System Function

6.1.5 Fight or Flight Response

6.1.6 The Brain (A2 only)

6.1.7 Localisation of Brain Function (A2 only)

6.1.8 Studying the Brain (A2 only)

6.1.9 CIMT (A2 Only) & Postmortem Examinations

6.1.10 Biological Rhythms (A2 only)

6.1.11 Studies on Biological Rhythms (A2 Only)

6.1.12 End of Topic Test - Biopsychology

6.1.13 Top Grade AO2/AO3 - Biopsychology

7 Research Methods

7.1 Research Methods

7.1.1 Experimental Method

7.1.2 Observational Techniques

7.1.3 Covert, Overt & Controlled Observation

7.1.4 Self-Report Techniques

7.1.5 Correlations

7.1.6 Exam-Style Question - Research Methods

7.1.7 End of Topic Test - Research Methods

7.2 Scientific Processes

7.2.1 Aims, Hypotheses & Sampling

7.2.2 Pilot Studies & Design

7.2.3 Questionnaires

7.2.4 Variables & Control

7.2.5 Demand Characteristics & Investigator Effects

7.2.6 Ethics

7.2.7 Limitations of Ethical Guidelines

7.2.8 Consent & Protection from Harm Studies

7.2.9 Peer Review & The Economy

7.2.10 Validity (A2 only)

7.2.11 Reliability (A2 only)

7.2.12 Features of Science (A2 only)

7.2.13 Paradigms & Falsifiability (A2 only)

7.2.14 Scientific Report (A2 only)

7.2.15 Scientific Report 2 (A2 only)

7.2.16 End of Topic Test - Scientific Processes

7.3 Data Handling & Analysis

7.3.1 Types of Data

7.3.2 Descriptive Statistics

7.3.3 Correlation

7.3.4 Evaluation of Descriptive Statistics

7.3.5 Presentation & Display of Data

7.3.6 Levels of Measurement (A2 only)

7.3.7 Content Analysis (A2 only)

7.3.8 Case Studies (A2 only)

7.3.9 Thematic Analysis (A2 only)

7.3.10 End of Topic Test - Data Handling & Analysis

7.4 Inferential Testing

7.4.1 Introduction to Inferential Testing

7.4.2 Sign Test

7.4.3 Piaget Conservation Experiment

7.4.4 Non-Parametric Tests

8 Issues & Debates in Psychology (A2 only)

8.1 Issues & Debates in Psychology (A2 only)

8.1.1 Culture Bias

8.1.2 Sub-Culture Bias

8.1.3 Gender Bias

8.1.4 Ethnocentrism

8.1.5 Cross Cultural Research

8.1.6 Free Will & Determinism

8.1.7 Comparison of Free Will & Determinism

8.1.8 Reductionism & Holism

8.1.9 Reductionist & Holistic Approaches

8.1.10 Nature-Nurture Debate

8.1.11 Interactionist Approach

8.1.12 Nature-Nurture Methods

8.1.13 Nature-Nurture Approaches

8.1.14 Idiographic & Nomothetic Approaches

8.1.15 Socially Sensitive Research

8.1.16 End of Topic Test - Issues and Debates

9 Option 1: Relationships (A2 only)

9.1 Relationships: Sexual Relationships (A2 only)

9.1.1 Sexual Selection & Human Reproductive Behaviour

9.1.2 Intersexual & Intrasexual Selection

9.1.3 Evaluation of Sexual Selection Behaviour

9.1.4 Factors Affecting Attraction: Self-Disclosure

9.1.5 Evaluation of Self-Disclosure Theory

9.1.6 Self Disclosure in Computer Communication

9.1.7 Factors Affecting Attraction: Physical Attributes

9.1.8 Matching Hypothesis Studies

9.1.9 Factors Affecting Physical Attraction

9.1.10 Factors Affecting Attraction: Filter Theory 1

9.1.11 Factors Affecting Attraction: Filter Theory 2

9.1.12 Evaluation of Filter Theory

9.1.13 End of Topic Test - Sexual Relationships

9.2 Relationships: Romantic Relationships (A2 only)

9.2.1 Social Exchange Theory

9.2.2 Evaluation of Social Exchange Theory

9.2.3 Equity Theory

9.2.4 Evaluation of Equity Theory

9.2.5 Rusbult’s Investment Model

9.2.6 Evaluation of Rusbult's Investment Model

9.2.7 Relationship Breakdown

9.2.8 Studies on Relationship Breakdown

9.2.9 Evaluation of Relationship Breakdown

9.2.10 End of Topic Test - Romantic relationships

9.3 Relationships: Virtual & Parasocial (A2 only)

9.3.1 Virtual Relationships in Social Media

9.3.2 Evaluation of Reduced Cues & Hyperpersonal

9.3.3 Parasocial Relationships

9.3.4 Attachment Theory & Parasocial Relationships

9.3.5 Evaluation of Parasocial Relationship Theories

9.3.6 End of Topic Test - Virtual & Parasocial Realtions

10 Option 1: Gender (A2 only)

10.1 Gender (A2 only)

10.1.1 Sex, Gender & Androgyny

10.1.2 Gender Identity Disorder

10.1.3 Biological & Social Explanations of GID

10.1.4 Biological Influences on Gender

10.1.5 Effects of Hormones on Gender

10.1.6 End of Topic Test - Gender 1

10.1.7 Kohlberg’s Theory of Gender Constancy

10.1.8 Evaluation of Kohlberg's Theory

10.1.9 Gender Schema Theory

10.1.10 Psychodynamic Approach to Gender Development 1

10.1.11 Psychodynamic Approach to Gender Development 2

10.1.12 Social Approach to Gender Development

10.1.13 Criticisms of Social Theory

10.1.14 End of Topic Test - Gender 2

10.1.15 Media Influence on Gender Development

10.1.16 Cross Cultural Research

10.1.17 Childcare & Gender Roles

10.1.18 End of Topic Test - Gender 3

11 Option 1: Cognition & Development (A2 only)

11.1 Cognition & Development (A2 only)

11.1.1 Piaget’s Theory of Cognitive Development 1

11.1.2 Piaget's Theory of Cognitive Development 2

11.1.3 Schema Accommodation Assimilation & Equilibration

11.1.4 Piaget & Inhelder’s Three Mountains Task (1956)

11.1.5 Conservation & Class Inclusion

11.1.6 Evaluation of Piaget

11.1.7 End of Topic Test - Cognition & Development 1

11.1.8 Vygotsky

11.1.9 Evaluation of Vygotsky

11.1.10 Baillargeon

11.1.11 Baillargeon's studies

11.1.12 Evaluation of Baillargeon

11.1.13 End of Topic Test - Cognition & Development 2

11.1.14 Sense of Self & Theory of Mind

11.1.15 Baron-Cohen Studies

11.1.16 Selman’s Five Levels of Perspective Taking

11.1.17 Biological Basis of Social Cognition

11.1.18 Evaluation of Biological Basis of Social Cognition

11.1.19 Important Issues in Social Neuroscience

11.1.20 End of Topic Test - Cognition & Development 3

11.1.21 Top Grade AO2/AO3 - Cognition & Development

12 Option 2: Schizophrenia (A2 only)

12.1 Schizophrenia: Diagnosis (A2 only)

12.1.1 Classification & Diagnosis

12.1.2 Reliability & Validity of Diagnosis

12.1.3 Gender & Cultural Bias

12.1.4 Pinto (2017) & Copeland (1971)

12.1.5 End of Topic Test - Scizophrenia Diagnosis

12.2 Schizophrenia: Treatment (A2 only)

12.2.1 Family-Based Psychological Explanations

12.2.2 Evaluation of Family-Based Explanations

12.2.3 Cognitive Explanations

12.2.4 Drug Therapies

12.2.5 Evaluation of Drug Therapies

12.2.6 Biological Explanations for Schizophrenia

12.2.7 Dopamine Hypothesis

12.2.8 End of Topic Test - Schizoprenia Treatment 1

12.2.9 Psychological Therapies 1

12.2.10 Psychological Therapies 2

12.2.11 Evaluation of Psychological Therapies

12.2.12 Interactionist Approach - Diathesis-Stress Model

12.2.13 Interactionist Approach - Triggers & Treatment

12.2.14 Evaluation of the Interactionist Approach

12.2.15 End of Topic Test - Scizophrenia Treatments 2

13 Option 2: Eating Behaviour (A2 only)

13.1 Eating Behaviour (A2 only)

13.1.1 Explanations for Food Preferences

13.1.2 Birch et al (1987) & Lowe et al (2004)

13.1.3 Control of Eating Behaviours

13.1.4 Control of Eating Behaviour: Leptin

13.1.5 Biological Explanations for Anorexia Nervosa

13.1.6 Psychological Explanations: Family Systems Theory

13.1.7 Psychological Explanations: Social Learning Theory

13.1.8 Psychological Explanations: Cognitive Theory

13.1.9 Biological Explanations for Obesity

13.1.10 Biological Explanations: Studies

13.1.11 Psychological Explanations for Obesity

13.1.12 Psychological Explanations: Studies

13.1.13 End of Topic Test - Eating Behaviour

14 Option 2: Stress (A2 only)

14.1 Stress (A2 only)

14.1.1 Physiology of Stress

14.1.2 Role of Stress in Illness

14.1.3 Role of Stress in Illness: Studies

14.1.4 Social Readjustment Rating Scales

14.1.5 Hassles & Uplifts Scales

14.1.6 Stress, Workload & Control

14.1.7 Stress Level Studies

14.1.8 End of Topic Test - Stress 1

14.1.9 Physiological Measures of Stress

14.1.10 Individual Differences

14.1.11 Stress & Gender

14.1.12 Drug Therapy & Biofeedback for Stress

14.1.13 Stress Inoculation Therapy

14.1.14 Social Support & Stress

14.1.15 End of Topic Test - Stress 2

15 Option 3: Aggression (A2 only)

15.1 Aggression: Physiological (A2 only)

15.1.1 Neural Mechanisms

15.1.2 Serotonin

15.1.3 Hormonal Mechanisms

15.1.4 Genetic Factors

15.1.5 Genetic Factors 2

15.1.6 End of Topic Test - Aggression: Physiological 1

15.1.7 Ethological Explanation

15.1.8 Innate Releasing Mechanisms & Fixed Action Pattern

15.1.9 Evolutionary Explanations

15.1.10 Buss et al (1992) - Sex Differences in Jealousy

15.1.11 Evaluation of Evolutionary Explanations

15.1.12 End of Topic Test - Aggression: Physiological 2

15.2 Aggression: Social Psychological (A2 only)

15.2.1 Social Psychological Explanation

15.2.2 Buss (1963) - Frustration/Aggression

15.2.3 Social Psychological Explanation 2

15.2.4 Social Learning Theory (SLT) 1

15.2.5 Social Learning Theory (SLT) 2

15.2.6 Limitations of Social Learning Theory (SLT)

15.2.7 Deindividuation

15.2.8 Deindividuation 2

15.2.9 Deindividuation - Diener et al (1976)

15.2.10 End of Topic Test - Aggression: Social Psychology

15.2.11 Institutional Aggression: Prisons

15.2.12 Evaluation of Dispositional & Situational

15.2.13 Influence of Computer Games

15.2.14 Influence of Television

15.2.15 Evaluation of Studies on Media

15.2.16 Desensitisation & Disinhibition

15.2.17 Cognitive Priming

15.2.18 End of Topic Test - Aggression: Social Psychology

16 Option 3: Forensic Psychology (A2 only)

16.1 Forensic Psychology (A2 only)

16.1.1 Defining Crime

16.1.2 Measuring Crime

16.1.3 Offender Profiling

16.1.4 Evaluation of Offender Profiling

16.1.5 John Duffy Case Study

16.1.6 Biological Explanations 1

16.1.7 Biological Explanations 2

16.1.8 Evaluation of the Biological Explanation

16.1.9 Cognitive Explanations

16.1.10 Moral Reasoning

16.1.11 Psychodynamic Explanation 1

16.1.12 Psychodynamic Explanation 2

16.1.13 End of Topic Test - Forensic Psychology 1

16.1.14 Differential Association Theory

16.1.15 Custodial Sentencing

16.1.16 Effects of Prison

16.1.17 Evaluation of the Effects of Prison

16.1.18 Recidivism

16.1.19 Behavioural Treatments & Therapies

16.1.20 Effectiveness of Behavioural Treatments

16.1.21 Restorative Justice

16.1.22 End of Topic Test - Forensic Psychology 2

17 Option 3: Addiction (A2 only)

17.1 Addiction (A2 only)

17.1.1 Definition

17.1.2 Brain Neurochemistry Explanation

17.1.3 Learning Theory Explanation

17.1.4 Evaluation of a Learning Theory Explanation

17.1.5 Cognitive Bias

17.1.6 Griffiths on Cognitive Bias

17.1.7 Evaluation of Cognitive Theory (A2 only)

17.1.8 End of Topic Test - Addiction 1

17.1.9 Gambling Addiction & Learning Theory

17.1.10 Social Influences on Addiction 1

17.1.11 Social Influences on Addiction 2

17.1.12 Personal Influences on Addiction

17.1.13 Genetic Explanations of Addiction

17.1.14 End of Topic Test - Addiction 2

17.2 Treating Addiction (A2 only)

17.2.1 Drug Therapy

17.2.2 Behavioural Interventions

17.2.3 Cognitive Behavioural Therapy

17.2.4 Theory of Reasoned Action

17.2.5 Theory of Planned Behaviour

17.2.6 Six Stage Model of Behaviour Change

17.2.7 End of Topic Test - Treating Addiction

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PAST PAPERS: AGGRESSION: AQA A-LEVEL PSYCHOLOGY RESOURCES

Psychology aqa   a level  unit 3: 7182/3.

Full model answers for all of these questions are  available here

Sign up to the PsychLogic newsletter at the bottom of this page to download printable AQA A-level Psychology revision notes + AQA A-level Psychology revision guide + A-level Psychology revision tips + more...

The best way to revise Psychology A-level

THE SYLLABUS

NEURAL AND HORMONAL MECHANISMS IN AGGRESSION

• The limbic system
• Serotonin and testosterone

GENETIC FACTORS IN AGGRESSION

• Twin and adoption studies
• The MAOA gene
• Evaluation of genetic factors

THE ETHOLOGICAL EXPLANATION OF AGGRESSION

• Innate releasing mechanisms and fixed action patterns
• Evolutionary explanations of human aggression

SOCIAL PSYCHOLOGICAL EXPLANATIONS OF HUMAN AGGRESSION

• The frustration-aggression hypothesis
• Social learning theory as applied to human aggression
• De-individuation

INSTITUTIONAL AGGRESSION

• Prisons & dispositional and situational explanations

MEDIA INFLUENCES ON AGGRESSION

• Television & computer games
• Desensitisation, Disinhibition, Cognitive priming

>>>>>>>

SPECIMEN PAPER 1 ( AQA A-level Psychology notes)

Read the item and then answer the questions that follow.

News correspondents in inner cities have remarked upon how young males frequently carry weapons and engage in threatening behaviour.

Using your knowledge of evolutionary explanations of aggression, account for these high levels of aggression in young males. [4 marks]

Briefly outline and evaluate the findings of one research study into genetic factors in aggression. [4 marks]

Describe and evaluate the social learning theory of human aggression. [16 marks]

SPECIMEN PAPER 2 ( A-level Psychology revision notes)

Discuss the role of genetic factors in aggression.

A psychologist was interested in the effects of violent computer games on aggression in young boys. Following appropriate ethical procedures she set up a study in which she identified ten boys who played violent computer games for at least two hours a day (Group A), and another group of ten boys who did not play violent computer games (Group B). The boys were systematically observed in their school playground on five separate occasions and the total number of aggressive behaviours they demonstrated was recorded. The data are given in Table 4 below:

Table 4: The effects of playing violent computer games on aggressive behaviour in boys

Complete Table 4 by calculating the median for the two groups. Why did the psychologist use the median as a measure of central tendency rather than the mean? [4 marks]

Briefly outline the possible role of cognitive priming in the effects of computer games on aggression. [2 marks]

Briefly explain one limitation of the situational explanation for institutional aggression. [2 marks]

 >>>>>>>

SPECIMEN PAPER 3 ( AQA A-level Psychology revision notes)

What are innate releasing mechanisms? [2 marks]

Discuss media influences on aggression. [8 marks]

A psychologist was investigating the effect of prison conditions on institutional aggression.

He selected a sample of 12 prisoners and counted the number of aggressive acts of each prisoner over one day in the exercise yard.

The prison conditions were then changed, such that the number of prisoners per cell was reduced and regular exercise periods introduced.

After three months of these new conditions the psychologist observed the same 12 prisoners and again counted the number of aggressive acts of each prisoner over one day in the exercise yard.

This study involves a repeated measures design.

Explain one advantage of using a repeated measures design in this study [2 marks]

The psychologist obtained the following results:

• For two of the prisoners the number of aggressive acts increased
• For eight of the prisoners the number of aggressive acts decreased
• For two of the prisoners the number of aggressive acts stayed the same

The psychologist decides to use a sign test to see if his data are significant.

What is the calculated value of the sign test statistic ‘S’? Explain your answer. [2 marks]

Look at the table of critical values of ‘S’ below and then answer the question that follows.

Using the table of critical values of ‘S’ above, state whether the findings of the study are significant at p < 0.05. Explain your answer. [2 marks]

Outline and evaluate the role of neural and/or hormonal mechanisms in aggression. [8 marks]

2017 (How to revise for A-level Psychology)

Briefly explain how cognitive priming in the media might influence aggressive behaviour. [2 marks]

A psychologist is investigating causes of aggressive behaviour. She interviews teenagers who have been in trouble at school. She asks them to describe their family and early childhood, recording everything that they say. She also looks at information in the teenagers’ school reports.

Referring to this investigation, explain the difference between primary and secondary data. [4 marks]

Explain how the psychologist could continue her investigation by carrying out thematic analysis of the interview recordings. [2 marks]

Describe and evaluate evolutionary explanations for human aggression. [16 marks]

2018 ( Psychology A-level revision)

Which two of the following statements are TRUE? Write the two correct letters in your answer book. [2 marks]

A           Aggression involves high MAOA gene activity

B           Aggression is influenced by the amygdala

C           The amygdala is located in the prefrontal cortex

D           The MAOA gene affects levels of testosterone

E           The MAOA gene influences levels of serotonin

Some people suggest that the media influences aggression through desensitisation. Evaluate desensitisation as an explanation for aggression [6 marks]

John was arrested for fighting with supporters of a rival team after a football match.

He explained to the police officer why he was aggressive. The police officer noted John’s comments in her notebook.

Table 5 below shows some of John’s comments.

• The players were fighting on the pitch
• Our team lost again – it’s not fair
• Supporters of the other team ganged up on us
• I was with my mates – we were all punching at once
• Everyone else was fighting, so I just joined in

Discuss one or more social psychological explanations for aggression. Refer to some of the comments in Table 5 in your answer. [16 marks]

2019 ( A-level Psychology revision)

A psychologist used a set of negative images to assess violent attitudes before and after participants played a 30-minute computer game. In a repeated measures design, 15 participants were tested before and after playing the game using a single set of images.

Explain how two sets of images could be used in this study and why this would be an improvement. [4 marks]

Each participant had a different total score in the before condition, where the maximum score was 40 and the median score was 23.

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• Published: 21 September 2018

Recent advances in the study of aggression

• Meghan E. Flanigan   ORCID: orcid.org/0000-0002-3185-7459 1 &
• Scott J. Russo   ORCID: orcid.org/0000-0002-6470-1805 1  

Neuropsychopharmacology volume  44 ,  pages 241–244 ( 2019 ) Cite this article

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Introduction

Aggression is an evolutionarily conserved behavior that controls social hierarchies and protects valuable resources like mates, food, and territory. In most cases, aggression is a normal and necessary component of social behavior. In humans, however, some forms of aggression are considered pathological behaviors that threaten lives, increase the likelihood of future psychiatric disease in victims and witnesses, and incur tremendous economic burdens on society [ 1 ]. Furthermore, while abnormal aggressive behavior is a symptom shared across a wide range of psychiatric and neurological diseases, there are few, if any, approved treatments aimed specifically at curbing it [ 2 ]. Despite the massive costs of violence on society, the pervasiveness of aggression among psychiatric patients, and our current lack of treatments, aggression historically has been understudied compared with other emotional behaviors in psychiatric patients [ 3 ]. While a recent surge in preclinical studies interrogating the neural circuitry underpinning aggression has provided important new findings regarding the brain regions, cell types, and neural ensembles governing specific components of this complex behavior, significant gaps in our understanding remain. In order to successfully develop novel treatments aimed at reducing aggression in a variety of patient populations, it is crucial that we address these gaps systematically, and with the consideration that aggressive behavior is influenced by an interconnected circuitry that integrates processes related to motivation, arousal, impulse control, memory, metabolism, sensory perception, and hormonal signaling, among others.

Recent advances in behavioral models of aggression

In order to investigate the neural circuit mechanisms underlying pathological aggressive behavior in humans, it is critical that researchers utilize animal models that fully capture the essential features of excessive human violence (see Table  1 ). Clinically, aggressive behavior is commonly classified as either proactive or reactive, and each of these classifications is generally associated with specific behavioral characteristics relevant to psychiatric disorders [ 4 ]. However, until recently, animal models of aggression have largely not distinguished between domains of behavior relevant to specific clinical subtypes of aggression. This may be an important reason for why our understanding of the neural circuitry of aggressive behavior remains tenuous.

Proactive aggression is commonly defined as aggression that is purposeful, goal-driven, and characterized by low emotional reactivity (hypoarousal). Under certain conditions, proactive aggression bears resemblance to drug addiction: aggression is sought compulsively despite adverse consequences (jail) and relapse to aggression following abstinence is common (recidivism) [ 5 ]. Consistent with this notion, researchers have recently developed animal models of aggression that are inspired by classical models of drug reward like self-administration and conditioned place preference (CPP) [ 6 , 7 , 8 , 9 ]. These models have been used to identify a handful of classical reward circuits that may be important for pathological aggression, and we argue for their widespread use in future investigations.

Reactive aggression is commonly defined as aggression that is impulsive, hostile, and characterized by high emotional reactivity (hyperarousal). Current animal models that are potentially relevant to reactive aggression include instigation/frustration models, alcohol exposure models, and anabolic steroid exposure models, as these models result in hyperarousal-associated aggression. However, it is important to note that in many humans and animal models, aggression cannot simply be defined as either proactive or reactive. Thus, it is important that animal models of aggression strive to recapitulate specific behavioral domains of proactive versus reactive aggression most relevant to those found in psychiatric patient populations.

Stepping outside of the VMH

A large portion of what we currently know about the circuitry governing aggression relates to the ventromedial hypothalamus (VMH), which was first identified as a site for driving the initiation of intermale attacks in the 1960s [ 10 ] (for review, see [ 11 ]). This focus has been driven by the idea that gaining a more detailed understanding of the control points for the expression of rodent species-typical aggressive behavior will promote the development of effective treatment strategies for humans displaying abnormal aggression [ 12 ]. Despite the appeal of this approach, there is scarce evidence that the VMH is involved in abnormal human aggression [ 4 ]. Rather, clinical neuroimaging studies have identified nuclei that are likely upstream of attack initiation nodes like the VMH as dysregulated in patients displaying aggression [ 13 ]. We argue that the wide range of aggressive behavior observed in human psychiatric patients is likely the result of aberrant activity within multiple neural circuits across the brain, each of which carry different streams of information that converge on attack initiation nuclei to control aggression. The development of effective treatments for aggression will require a deeper understanding of the functional connectivity and behavioral roles of each of these circuits in animal models that reflect the heterogeneity of aggressive behavior observed in human patients (see Table  1 ).

Influences of motivation on aggression

A growing number of studies in humans and animals illustrate that the propensity to carry out violent acts is influenced by the degree to which an individual finds aggression rewarding [ 14 ]. This suggests that neural circuits controlling the positive valence of aggressive social interactions are dysregulated in some patients displaying abnormal aggression, though it is unclear precisely how primary reward centers interact with aggression initiation circuitry. In support of this, neuroimaging studies in human psychiatric patients, particularly those with personality disorders, describe structural and functional abnormalities in key reward-related regions like the striatum that are correlated with aggression [ 15 , 16 ]. Consistent with human studies, recent investigations utilizing animal models of aggression CPP have identified functional roles for both the nucleus accumbens (NAc) [ 17 ] and the lateral habenula (LHb) [ 9 ] in the reinforcing effects of aggression. Interestingly, the VMH itself has also been reported to control aggression-seeking behavior in an operant model, indicating that this nucleus is not simply functioning as an on/off switch for attack, but may integrate information from primary reward centers to reinforce aggressive behavior [ 6 ]. A very recent study also found that the ventral premammillary nucleus (PMv) plays an important role in aggression and the establishment of social hierarchy via divergent projections to the supramammillary nucleus (SuM) and the VMH [ 18 ]. Although PMv inputs to the SuM promote aggression CPP without impacting aggression, PMv inputs to the VMH promote aggression without impacting aggression CPP. These results suggest that circuits controlling these two aspects of aggressive behavior (valence versus initiation) may be dissociable. Much work is required to determine how non-hypothalamic regions like the LHb and the NAc interface with the VMH or other aggression initiation circuits to promote aggression and its rewarding effects. Multisynaptic tracing and functional mapping studies will be important for determining this. In addition, we know that levels of aggression increase with repeated experience, a phenomenon akin to drug-induced sensitization, which is prominently regulated by reward circuits including the NAc and LHb. Thus, a key future question is how aggression experience shapes reward-related neural and behavioral responses to guide future aggressive interactions. Does aggression intensity mirror changes in the reward valence and is this associated with reward circuit plasticity? Understanding these important questions may be highly relevant for the treatment of extremely aggressive individuals exhibiting high rates of recidivism.

Influences of emotional reactivity and impulse control on aggression

Although some psychiatric patients exhibiting abnormal aggression do so because they find violence rewarding (termed proactive aggression, see previous section), others may do so because of inappropriate emotional reactivity to perceived social threats and poor impulse control (termed reactive aggression) [ 13 ]. Perhaps unsurprisingly, a large body of evidence suggests that the circuits controlling these two types of aggressive behavior differ significantly [ 4 ]. Clinical neuroimaging studies broadly suggest that reactive aggression involves simultaneous hypofunction of the medial prefrontal cortex (mPFC) and hyperfunction of the amygdala [ 13 ]. Activation of the amygdala and extended amygdala promotes aggression in a variety of animal models [ 19 ]. However, preclinical studies investigating the role of the mPFC in aggression appear conflicting. For example, there is evidence that optogenetic stimulation of the mPFC both reduces [ 20 ] and increases [ 21 , 22 , 23 ] aggression and dominance. These discrepant findings may be explained by differences in the animal models of aggression used. It is possible that mPFC hypofunction underlies reactive forms of aggression, whereas PFC hyperfunction underlies proactive forms of it. In addition, it may be that specific outputs from the mPFC play opposing roles in aggression such that broad manipulation of this nucleus provides inconsistent results. This idea is somewhat supported by a recent study that found differential roles for mPFC outputs to the mediobasal hypothalamus and lateral hypothalamus, which drive species-typical versus species atypical (escalated) aggression, respectively [ 24 ]. Future work should aim to functionally dissect the specific roles of mPFC cell types and their outputs in models of proactive versus reactive aggression. Furthermore, the downstream circuit mechanisms by which the mPFC and amygdala influence the initiation of aggression should be fully explored.

Influences of social context on aggression

Recent work suggests that circuits conveying information about social context influence the activity of attack nuclei. For example, the capacity for optogenetic stimulation of VMH neurons to initiate aggression is affected by whether residents and intruders are single or group housed prior to testing [ 25 ]. Although stimulation of VMH neurons is sufficient to drive aggression independently of pheromone sensing capabilities, gonadal hormone status, and physical cues indicating the presence of a conspecific in single-housed males, this manipulation is insufficient to initiate attack in group-housed males [ 25 , 26 ]. This suggests that VMH neurons may in fact be regulated by circuits conveying social context, such as those relevant to olfaction and ultrasonic vocalization. As VMH neurons have the capacity to distinguish male versus female conspecifics [ 27 ], it is possible that the VMH also encodes other social information about male conspecifics within a group, including their status in the social hierarchy, to control whether aggression is initiated. Mechanistic insights into this phenomenon may enable us to reduce violence in patients through the therapeutic normalization of circuits signaling whether aggression is appropriate in given social contexts.

Other factors influencing aggression

In many psychiatric patients, violent behaviors intensify during certain times of day, indicating that circadian circuits controlling arousal may be important modulators of VMH neurons driving aggression [ 28 ]. Though this effect has been well documented in clinical populations, only one recent study has investigated the relevant circuit mechanisms in an animal model of aggression [ 29 ]. Researchers found that there is indeed a daily rhythm of aggressive behavior in mice that resembles clinical patterns of aggression in psychiatric patients [ 29 ]. This rhythm appears to be controlled by a multisynaptic circuit from the suprachiasmatic nucleus to the VMH via the subventricular zone (SVZ). Inhibitory inputs to VMH neurons from the SVZ were found to be more active during the day than at night, thereby resulting in increased aggressive behavior in the early night. The findings of this study have potentially important implications for future studies on aggression, which will require the consideration of behavioral testing time in the design of experiments and interpretation of results. These results also suggest that psychiatric patients who display daily oscillations in aggressive behavior, such as those with Alzheimer’s disease or psychosis, may respond well to treatments targeting this circuit. It is very likely that other circuits conveying information about an individual’s internal state (hunger, thirst, etc.) are also playing roles in aggressive behavior, though these have yet to be explored.

Aggression in females

A central question that remains is whether the same circuits controlling aggression in males are involved in female aggression. Comparisons of the mechanisms of male and female aggression in animal models have classically proven difficult because of fundamental differences in the contexts in which males and females attack. However, a handful of recent studies have begun to investigate this. One recent study found that optogenetic activation of aromatase-positive neurons in the amygdala promotes both intermale aggression and maternal aggression [ 30 ]. Interestingly, optogenetic stimulation of VMH neurons promotes aggression in intact, but not ovariectomized females [ 25 , 31 , 32 ], suggesting that unlike in males, female gonadal hormone signaling is downstream of VMH. Moreover, although VMH neural ensembles encoding sexual versus aggressive behavior appear to largely overlap in males, these populations display little overlap in females [ 31 ]. These differences in VMH circuitry, as well as potential differences in the contributions of various inputs to VMH neurons of males and females, should be explored. It also remains unknown whether recent findings describing the capacity for male rodents to be highly reinforced by aggression extends to females. Considering the propensity for women, particularly those with neuropsychiatric disorders, to carry out premeditated violent acts [ 33 ], it is crucial that the field extends its efforts to interrogate underlying circuit mechanisms of reward, if any, in female animal models of aggression.

Conclusions

In order to develop more effective treatments for neuropsychiatric illnesses marked by heightened aggression, we must consider the fact that aggression symptoms in clinical populations take various forms, which likely involve different mechanisms and underlying circuitry. For example, while treatments for patients with personality disorders may require reducing the valence of aggression to prevent future violent acts, treatments for aggressive patients with Alzheimer’s disease may require a normalization of circadian dysfunction. Patients who display reactive aggression, such as those with Intermittent Explosive disorder, may require treatments that improve function in circuits controlling behavioral inhibition and top–down impulse control. Moreover, there are clear sex differences in aggression that we need to better understand before we can adequately address aggression circuitry in men versus women. Ultimately, our ability to develop personalized treatments for the broad array of aggressive disorders will require the systematic utilization of a variety of animal models, informed by studies of human illness, which recapitulate specific etiological factors driving aggressive behavior.

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Acknowledgements

The authors are supported by NIH grants 1R01MH114882-01 (SJR) and F31 MH111108-01A1 (MEF).

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Flanigan, M.E., Russo, S.J. Recent advances in the study of aggression. Neuropsychopharmacol 44 , 241–244 (2019). https://doi.org/10.1038/s41386-018-0226-2

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Study Notes

Aggression: Evaluating Dispositional Explanations

Last updated 22 Mar 2021

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The study notes follow on from the 'Aggression: Dispositional Explanations ' notes.

Adams (1981) found that in American prisons, black inmates were more likely to be associated with violent acts in comparison to white inmates. The argument for this is that black prisoners tended to come from poorer backgrounds with higher rates of crime, and so imported their cultural norms into the prison supporting the dispositional explanation of aggression.

Gaes et al. (1988) studied 82,000 prisoners in US prisons and found prisoners with Hispanic origins were more violent than those with a non-Hispanic origin. Also prisoners with Asian origins were less likely to be violent than those who were non-Asian. This research supports the view that culture and consequently ethnicity are factors that can contribute to aggression being imported into the prison institution.

However, DeLisi (2004) studied 813 male inmates in US prisons and found no correlation between violence in prisons and previous gang membership. Therefore, there is conflicting research support for the dispositional explanation. The importation model predicts that violence and aggression is introduced by individuals with a culture of aggression in their lives. It would be expected that gang members would be more likely to display aggression inside prisons, but DeLisi (2004) found no evidence to support this prediction.

Most of the research has been undertaken on male prisoners so very little is known about reasons for female violence in prisons. It would be androcentric to presume the same reasons for male violence can be used to explain female violence. There may be other factors involved that can result in female prison aggression. Therefore, the research can be accused of exhibiting a beta bias. It may be that males import aggression into the prison environment, but there may be differences to the extent that dispositional or situational factors affect each gender.

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