Individual Differences Chapter 5 and 6

What is a personal construct?

A bipolar mental category (e.g., safe–dangerous) used to interpret the world.

What are schemas?

Organised mental frameworks guiding thought and behaviour.

What is attributional style?

Habitual way of explaining events (internal/external, stable/unstable, global/specific).

What is self-efficacy?

Belief in one’s ability to perform successfully in a given context.

Who created the Rep Test and what does it measure?

George Kelly; measures personal constructs.

What is Beck’s negative triad?

Negative views of self, world, future.

What did Seligman’s learned helplessness experiments show?

Uncontrollable events → passivity; linked to pessimistic attributional style.

What is the “personality coefficient”?

Mischel’s finding that traits correlate weakly (r ≈ .30) with behaviour.

One strength and one weakness of Kelly’s personal construct theory?

Strength = captures idiographic meaning; Weakness = not easily testable.

How does attributional style link to mental health?

Pessimistic style predicts depression; optimistic style predicts resilience.

How does Bandura’s concept of reciprocal determinism explain personality?

Behaviour, cognition, and environment influence each other bidirectionally.

Why is CAPS significant?

Integrates traits + situations; explains consistency paradox.

Evaluate cognitive approaches to personality.

Strengths: focus on cognition, practical applications (therapy, positive psych). Weaknesses: reductionist, difficult to falsify, underestimates biology. Compare Kelly (idiographic) vs Bandura (empirical, measurable self-efficacy).

What is heritability of personality traits?

About 40–60% of variance explained by genetics.

What are Eysenck’s three personality dimensions?

Psychoticism, Extraversion, Neuroticism.

What does BIS stand for?

Behavioural Inhibition System.

Which neurotransmitter is linked with novelty seeking?

Dopamine.

What did Bouchard’s twin study show?

Twins reared apart still have strong personality correlations → genetic influence.

What did Geen (1984) find about introverts vs extraverts?

Introverts prefer lower noise levels, extraverts prefer higher.

What does Canli et al. (2001) show about neuroticism?

Higher amygdala activation to negative stimuli.

Strength of Eysenck’s model?

Parsimonious, testable biological basis.

Weakness of Cloninger’s model?

Complex, difficult to test empirically.

Problem with biological reductionism?

Ignores environmental and cognitive influences.

Evaluate Gray’s RST vs Eysenck’s PEN model.

Eysenck = simple, linked to cortical arousal & limbic system, but oversimplified. Gray = more precise neural mechanisms, explains anxiety/impulsivity better, but complex revisions reduce clarity.

Discuss genetic and neurobiological evidence for personality.

Twin studies show heritability; neurotransmitters (dopamine, serotonin) linked to traits; fMRI supports links. Evaluation: strong methods, but reductionist and may overstate determinism.

What is heritability?

% of variance due to genetic differences in a population (not fate for an individual).

Name the three RST systems.

BAS, BIS, FFFS (approach, anxiety/conflict, fear).

What are Cloninger’s temperament vs character groups?

Temperament: Novelty Seeking, Harm Avoidance, Reward Dependence, Persistence; Character: Self-Directedness, Cooperativeness, Self-Transcendence.

Define sensation seeking.

Preference for novel/intense experiences + risk willingness.

Eysenck’s arousal hypothesis for Extraversion?

Introverts higher baseline cortical arousal; extraverts lower → seek stimulation.

One neural correlate for Neuroticism?

Greater amygdala reactivity to threat/negative affect.

Why did candidate gene studies fall out of favour?

Poor replication; personality is polygenic with tiny single-variant effects.

What does BIS predict vs BAS?

BIS → anxiety/avoidance; BAS → reward-drive/impulsivity/positive affect.

Give one rGE type with example.

Active rGE: thrill-seeking teen chooses extreme sports, amplifying trait.

How can G×E change trait expression?

Stressful environments can magnify genetic risk for high Neuroticism.

One strength of biological approaches?

Objective tools (twin designs, imaging, GWAS) give mechanistic traction.

One core limitation?

Reductionism: small effects; environment/learning massively shape outcomes.

What’s the network (systems) lesson from imaging?

Traits emerge from distributed, interacting circuits, not single loci.

How do biological and social-cognitive models fit together?

Biology sets propensities; environments and self-regulation shape expression.

Compare Eysenck’s PEN and Gray’s RST.

Eysenck: arousal (ARAS), limbic reactivity; simple axes (E, N, P); clear predictions. Gray: motivational systems (BAS/BIS/FFFS) → better mapping to reward/threat; clinical relevance for anxiety/impulsivity. Evidence: mixed for pure arousal; stronger for reward/threat circuits. Conclusion: RST refines mechanisms; PEN remains historically important.

“Personality is genetic.” Discuss.

For: h² ~ .40–.50; twin/adoption; cross-cultural stability. Against: G×E, rGE; small polygenic effects; powerful environmental shaping; interventions work. Nuanced conclusion: genetically influenced, not genetically fixed.

Is Cloninger’s model useful clinically?

For: integrates temperament + character; psychiatric links; TCI used clinically. Against: complexity; debated transmitter mappings; measurement variance. Verdict: useful framework, but mechanistic claims should be cautious.