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What is localization of function?
The idea that particular brain regions perform specialized functions. Example: hippocampal damage can impair formation of new long-term memories.
What is neuroplasticity?
The brain's capacity to change structurally or functionally through experience, learning or environmental influences. Example: learning a skill can alter neural connections.
What is a neurotransmitter?
A chemical messenger released by neurons that influences communication between cells. Example: serotonin is involved in mood regulation and has been investigated in aggression.
What is a hormone?
A chemical messenger released by endocrine glands into the bloodstream, influencing target tissues and behaviour. Example: testosterone has been studied in relation to aggression.
What is a pheromone?
A chemical signal released by an organism that may influence behaviour or physiological responses in another member of the same species. Human pheromone effects remain debated.
What is genetic similarity?
The degree to which individuals share genetic material. Twin and kinship studies examine whether greater relatedness is associated with similarities in behaviour.
What is an evolutionary explanation of behaviour?
Explains behaviour through natural selection: characteristics that improve reproductive success may become more common across generations. Example: proposed adaptive functions of fear.
What is gene–environment interaction?
The effect of genetic differences on behaviour may depend on environmental exposure, and environmental effects may vary with genetic characteristics. Example: MAOA variation and childhood maltreatment.
What is epigenetics?
Changes in gene expression that do not require changes to the underlying DNA sequence. Environmental experiences can influence whether particular genes are expressed.
How does fMRI investigate brain–behaviour relationships?
It measures blood-oxygen-level-dependent signals as an indirect indicator of neural activity. It can identify activity associated with a task but cannot, alone, prove causation.
What does an MRI measure?
Magnetic resonance imaging produces structural images of the brain. Researchers can compare anatomy, such as hippocampal volume, between individuals or groups.
What is reductionism in biological psychology?
Explaining complex behaviour primarily through biological mechanisms. Strength: generates testable explanations; limitation: may understate cognitive, social and cultural influences.
What is biological determinism?
The claim that behaviour is determined by biological factors. A strong deterministic interpretation can overlook agency, learning and environmental influences.
What is the main limitation of correlational brain research?
Brain activity and behaviour may be associated without one causing the other. Confounding variables and reverse causation may offer alternative explanations.
How does animal research help biological psychology?
It permits controlled investigation of mechanisms that may be difficult to study in humans. However, species differences limit generalization and animal welfare must be protected.
What are the key ethical concerns in animal research?
Minimize pain and distress, justify scientific value, use alternatives where possible, and apply replacement, reduction and refinement. Potential human benefits do not automatically justify suffering.
What was Bechara et al. (2000) investigating?
Aim: investigate decision-making deficits associated with ventromedial prefrontal cortex (vmPFC) damage. Method: human lesion research using a gambling task. Findings linked vmPFC damage with impaired advantageous decision-making. Supports localization, but lesion studies cannot isolate every contributing mechanism. Exact sample details: [verify].
How does Bechara et al. (2000) support localization?
The decision-making difficulties associated with vmPFC damage support a role for this region in decision-making. However, damage may affect connected networks, so the evidence does not establish that one region alone controls decisions.
What did Urry et al. (2006) investigate?
Aim: examine prefrontal regulation of the amygdala and its relationship with cortisol in older adults. Method: correlational neuroimaging and cortisol measurements. Findings linked greater ventromedial prefrontal activity with lower amygdala activity and lower cortisol. Supports emotion regulation, but correlation cannot establish causation. Sample and exact statistics: [verify].
How does Urry et al. (2006) complement localization research?
It links vmPFC activity to amygdala regulation and cortisol, extending localization beyond decision-making to emotion regulation. Together with Bechara et al., it suggests that brain regions contribute to different functions within interacting neural systems.
What did Feinstein et al. (2011) investigate?
Aim: examine fear in a person with bilateral amygdala damage. Method: detailed case study of patient SM using real-life and laboratory fear-provoking situations. Findings showed unusually limited fear responses in several situations. Supports an amygdala role in fear, but one unusual case limits generalizability. Exact procedural details: [verify].
What is a limitation of Feinstein et al. (2011)?
SM was a single, unusual case, so findings may not generalize to everyone. Amygdala damage may also affect connected systems. The study supports a role in fear but does not show that all fear depends exclusively on the amygdala.
What did Scoville and Milner (1957) investigate?
Aim: examine memory following medial temporal lobe surgery. Method: case study of patient H.M. after bilateral medial temporal lobe removal. Findings: severe anterograde amnesia with some preserved abilities. Supports a role for medial temporal structures in forming new declarative memories; one case limits generalization. Exact clinical details: [verify].
How does Scoville and Milner (1957) support localization?
H.M.'s inability to form many new long-term memories after surgery linked medial temporal structures to memory formation. Preserved abilities showed that memory is not a single process located in one structure.
What did Luby et al. (2013) investigate?
Aim: investigate associations between childhood poverty and brain development. Method: longitudinal research with children, assessing socioeconomic circumstances and brain structure. Findings linked poverty with differences in brain development, partly associated with caregiving and stressful experiences. Supports environmental influences on neurodevelopment, but observational evidence cannot prove poverty directly caused the differences. Exact sample/statistics: [verify].
How does Luby et al. (2013) illustrate neuroplasticity?
Associations between childhood socioeconomic adversity and brain development suggest that environmental experiences relate to neural development. However, the study does not establish that every observed difference reflects plasticity or that poverty alone caused it.
What did Passamonti et al. (2012) investigate?
Aim: investigate serotonin and neural responses related to aggression. Method: experimental manipulation of serotonin availability with fMRI during emotional processing. Findings linked reduced serotonin availability with altered neural responses to angry faces. Supports a neurochemical contribution to aggression-related processing, but neural responses are not equivalent to actual aggressive behaviour. Sample/statistics: [verify].
What is a limitation of Passamonti et al. (2012)?
An experimental manipulation strengthens causal inference about serotonin availability and measured responses. However, laboratory responses to emotional faces may not predict real-world aggression, and the effects of a temporary manipulation may not represent chronic differences.
What did Radke et al. (2015) investigate?
The relationship between testosterone and aggression-related behaviour. The uploaded study list identifies it as evidence for hormones and aggression. Use the exact procedure, sample, results and statistics only after checking the original paper: [verify].
What did Caspi et al. (2002) investigate?
Aim: test whether MAOA genotype moderated the relationship between childhood maltreatment and later antisocial behaviour. Method: longitudinal research involving 442 male members of a birth cohort. Findings: maltreatment was more strongly associated with antisocial outcomes among males with low-MAOA activity. Supports gene–environment interaction, not genetic inevitability.
How does Caspi et al. (2002) challenge genetic determinism?
The findings suggest that the association between maltreatment and antisocial outcomes varied by MAOA activity. Neither genotype nor maltreatment alone fully explained the pattern, supporting interaction rather than a single predetermined cause.
What did Gilbertson et al. (2002) investigate?
Aim: investigate genetic vulnerability to PTSD using twins. Method: twin comparisons involving Vietnam-era combat veterans and their co-twins. Findings linked smaller hippocampal volume with PTSD vulnerability, including in some unexposed co-twins. This supports a possible pre-existing vulnerability, but does not establish that hippocampal volume alone causes PTSD. Exact sample/statistics: [verify].
How does Gilbertson et al. (2002) complement Caspi et al. (2002)?
Both investigate biological vulnerability in interaction with life experience. Caspi examines genetic moderation of maltreatment effects; Gilbertson examines hippocampal volume and PTSD vulnerability. Together they challenge explanations based exclusively on genes or environment.
Evaluate the use of fMRI in biological psychology.
Strengths: non-invasive, provides spatial information and measures activity during tasks. Limitations: activity is an indirect signal; reverse inference and correlational designs weaken causal claims. Application: helps researchers investigate brain systems involved in emotion, memory and decision-making.
Describe one study of localization of function. (PEEL)
Point: brain regions have specialized roles. Evidence: Scoville and Milner (1957) studied H.M. after medial temporal lobe surgery. Explain: his severe anterograde amnesia implicated these structures in forming new memories. Link: this supports localization while showing memory involves distinguishable processes.
Explain neuroplasticity using one study. (PEEL)
Point: experience and environmental conditions relate to brain development. Evidence: Luby et al. (2013) linked childhood poverty with differences in brain development. Explain: stress and caregiving may help account for these associations. Link: the findings are consistent with environmental influences on neural development, but do not prove causation.
Discuss the role of neurotransmitters in behaviour. (SEEL)
Statement: neurotransmitters can influence behaviour-related processes. Evidence: Passamonti et al. (2012) investigated serotonin availability and neural responses to angry faces. Explain: this supports a neurochemical contribution to aggression-related processing. Evaluation: laboratory neural responses are not equivalent to real aggression. Link: neurotransmitters contribute to, but do not wholly explain, behaviour.
Evaluate the biological approach to behaviour. (PEEL)
Point: biological explanations are testable and supported by physiological evidence. Evidence: Bechara et al. linked vmPFC damage with decision-making deficits. Explain: lesion and neuroimaging evidence can identify brain–behaviour relationships. Evaluation: reductionism, confounding variables and limited generalizability restrict conclusions. Link: integrate biological findings with cognitive and sociocultural explanations.
To what extent does genetics explain behaviour? (SEEL)
Statement: genetic factors can contribute to behavioural differences, but do not determine every outcome. Evidence: Caspi et al. (2002) found that MAOA activity moderated the association between maltreatment and antisocial outcomes. Explain: this supports gene–environment interaction. Evaluation: one cohort and one gene–environment relationship cannot explain all behaviour. Link: biological vulnerability must be considered alongside experience.