BioPsychology Flashcards

(34 cards)

1
Q

Why might the fight or flight response be maladaptive in modern life?

A

It evolved for survival in physical threats but is over-activated by modern stressors (e.g. work). Chronic activation increases blood pressure, raising risks of heart disease.

Highlights mismatch between evolved mechanisms and current environments.

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2
Q

How is the fight or flight response potentially biased in gender representation?

A

Taylor et al. (2000): women may show a “tend and befriend” response due to evolutionary pressure to protect offspring and seek social support.

Suggests beta bias in assuming universality across genders.

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3
Q

What cognitive theory challenges the automaticity of fight or flight?

A

Lazarus (1990) argued that perception/appraisal of threat determines stress response.

Cognitive appraisal (e.g. threat vs. challenge) affects intensity of physiological reaction.

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4
Q

What are long-term health implications of prolonged fight or flight activation?

A

Chronic stress activates the sympathetic nervous system repeatedly.

Can damage cardiovascular system and suppress immune function over time

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5
Q

What brain imaging evidence supports localisation of function?

A

Peterson et al. (1988): Broca’s area active during reading, Wernicke’s during listening. Tulving et al. (1994): semantic & episodic memories localised in different areas of the prefrontal cortex.

Brain scans provide scientific support.

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6
Q

What does Phineas Gage’s case suggest about localisation?

A

Damage to frontal lobe led to major personality changes.

Supports the idea that specific regions (e.g. prefrontal cortex) regulate certain behaviours (e.g. decision-making/emotion).

Counterpoint: Case studies may lack generalisability and control over variables.

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7
Q

What is a major challenge to localisation theory from animal research?

A

Lashley (1950): Removing 10–50% of cortex in rats learning mazes didn’t impair learning. Suggests functions like learning are distributed.

Supports holistic theory for complex tasks.

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8
Q

How has localisation theory informed treatments?

A

Dougherty et al. (2002): 32-45% of OCD patients improved after cingulotomy.

Shows that understanding specific brain regions leads to targeted interventions.

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9
Q

What did Sperry’s split-brain research show?

A

Left hemisphere = verbal/language; right = visual-spatial processing.

Demonstrates hemispheric specialisation.

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10
Q

What are the limitations of split-brain research?

A

Small sample size (11); epilepsy history & surgical differences = confounding variables.

Limits generalisability & internal validity.

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11
Q

How has lateralisation been oversimplified in popular psychology?

A

Nielsen et al. (2013): brain scans of 1000 people found no dominant hemisphere.

Suggests the brain is more integrated than strict lateralisation implies.

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12
Q

What are the real-world contributions of split-brain research?

A

Supports localisation theories & inspires debate about ‘dual minds’ (Pucetti, 1980).

Advanced understanding of hemisphere function despite challenges.

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13
Q

What research supports brain plasticity?

A

Maguire et al. (2000): London taxi drivers = larger posterior hippocampus. Draganski et al. (2006): medical students’ brains changed post-exam.

Shows structure changes with experience.

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14
Q

How does functional recovery manifest after trauma?

A

Axonal sprouting, recruitment of homologous areas. Case studies (e.g. EB) & animal models support post-injury reorganisation.

Demonstrates brain’s adaptability.

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15
Q

Is plasticity possible in adulthood?

A

Bezzola et al. (2012): 40 hours of golf training changed motor cortex in 40–60 year olds.

Suggests neuroplasticity continues later in life.

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16
Q

What are the negative effects of brain plasticity?

A

Phantom limb syndrome (60–80% of amputees). Drug abuse leads to harmful brain changes.

Plasticity can have maladaptive outcomes.

17
Q

What is fMRI and what are its strengths and weaknesses?

A

Functional Magnetic Resonance Imaging (fMRI) detects changes in blood oxygenation and flow in active brain areas (haemodynamic response).

Non-invasive, high spatial resolution (1–2 mm), good for localisation
– Poor temporal resolution (~5s delay), expensive

18
Q

What is EEG and what are its strengths and limitations?

A

Electroencephalogram (EEG) measures electrical activity via electrodes on the scalp. Detects synchronous firing of neurons.

High temporal resolution (milliseconds), useful for sleep/epilepsy studies
– Low spatial resolution, can’t locate deep activity

19
Q

What are ERPs and how are they used?

A

Event-Related Potentials (ERPs) are brainwaves linked to specific stimuli. Derived from EEG by averaging signals.

High temporal resolution; used in attention/perception research
– Prone to noise; lack standardisation across studies

20
Q

What is a post-mortem exam and what are its pros/cons?

A

ost-mortem = analysis of brain after death to identify abnormalities linked to behaviour.

Informs early localisation (e.g. Broca’s area), useful for rare conditions
– No causality, ethical issues with consent, retrospective

21
Q

What is the SCN and what role does it play?

A

The Suprachiasmatic Nucleus (SCN) is a bundle of nerve cells in the hypothalamus that regulates circadian rhythms. It receives light info from the optic nerve and adjusts melatonin production by the pineal gland.

SCN = primary endogenous pacemaker

22
Q

What evidence supports the SCN’s role in circadian rhythms?

A

DeCoursey et al. (2000): SCN-lesioned chipmunks lost rhythms and had higher death rates. Ralph et al. (1990): mutant SCN transplanted into normal hamsters changed their cycles.

SCN is key to rhythm regulation

Counterpoint: Findings may not generalise to humans; ethical issues in animal research

23
Q

What are the strengths and limitations of circadian rhythm studies?

A

Practical applications to shift work and chronotherapeutics (e.g. heart meds timed for dawn). Limitation: Studies like Siffre allowed artificial light (a zeitgeber), and Damiola showed liver clocks shift independently of SCN.
Multiple internal clocks exist beyond SCN

24
Q

How do exogenous zeitgebers affect sleep-wake cycles?

A

Campbell & Murphy (1998): light on knees altered sleep cycles without eye input. Shows peripheral detection possible.

Counterpoint: Arctic dwellers maintain rhythms despite darkness; Miles et al. (1977) case of blind man with 24.9h cycle supports sunlight via eyes as key entrainer.

25
Infradian and Ultradian rhythms: Support from Stern & McClintock (1998) – Menstrual Synchrony
Stern and McClintock found that menstrual cycles may be influenced by external pheromones, showing a role for exogenous cues in infradian rhythms. They collected pheromones from 9 women and applied them to 20 others with irregular cycles. 68% of women experienced changes that aligned their cycle more closely to their ‘odour donor’, suggesting that the menstrual cycle, while endogenous, can be entrained by exogenous factors. 🔍 This supports the idea that infradian rhythms are not purely internal and can be influenced socially or chemically.
26
But, contradictory menstrual research
Trevathan et al. found no evidence of menstrual synchronisation in an all-female sample, contradicting McClintock’s findings. This suggests the influence of pheromones may be overstated or dependent on confounding variables. Since McClintock didn’t control for factors like smoking, exercise, or stress, the synchrony may have been coincidental or due to lifestyle similarities rather than pheromonal influence. 🔍 This questions the reliability of the findings and the strength of pheromones as zeitgebers.
27
Ultradian Rhythms, Kleitman
Dement and Kleitman monitored 33 adults under controlled conditions using EEGs. They found consistent evidence for REM sleep, with rapid eye movements occurring in every night of undisturbed sleep. When participants were woken during REM, they could recall dreams more accurately. 🔍 This confirms that sleep cycles (an ultradian rhythm) follow predictable brainwave patterns and stages, supporting the theory of ultradian rhythms with robust physiological evidence.
28
Sleep stages and menstrual duration vary by age
Although both infradian and ultradian rhythms follow identifiable patterns, not all individuals experience a textbook 28-day menstrual cycle or 90-minute sleep cycle. Sleep stages and menstrual duration can vary due to age, lifestyle, stress, or genetics. 🔍 This means while the biological model is useful, it may oversimplify the complex, variable nature of biological rhythms, making it less universally applicable.
29
Endogenous influence, Siffre
Michel Siffre spent long periods in caves without light or time cues. His sleep-wake cycle settled to around 24–25 hours, slightly longer than a natural day, showing that we have an internal pacemaker (the SCN) that maintains a rhythm without external input. 🔍 This supports the idea of a strong endogenous influence but also shows the need for exogenous cues to fine-tune it to exactly 24 hours.
30
SCNs role as endogenous pacemaker, Morgan
Morgan bred hamsters with 20-hour circadian rhythms and transplanted their SCNs into normal hamsters. After the transplant, the normal hamsters adopted the 20-hour rhythm, showing that the SCN controls circadian timing. 🔍 This demonstrates the SCN’s crucial role as an endogenous pacemaker in maintaining biological rhythms.
31
Infant Rhythms Entrained by Social Cues
Newborns initially show random sleep-wake cycles. By 6 weeks, rhythms begin to appear, and by 16 weeks, these become entrained, largely due to parental-imposed routines like feeding and sleeping schedules. 🔍 This supports the importance of exogenous zeitgebers (social cues) in fine-tuning biological rhythms early in life.
32
Jet Lag and Zeitgebers
Research suggests adjusting to local meal and sleep times helps entrain circadian rhythms after long-distance travel. This shows practical application of exogenous zeitgebers in managing circadian disruption like jet lag. 🔍 However, the reliance on light as the main zeitgeber may be overstated. Other factors (social interactions, temperature) likely play a role, meaning the model may be too reductionist.
33
Difference between the Sleep-Wake cycle and Stages of Sleep?
The sleep-wake cycle as a whole is a circadian rhythm because it follows a roughly 24-hour cycle and is influenced by the SCN (suprachiasmatic nucleus) and light levels. The stages of sleep within each sleep period (Stages 1–4 and REM) form a sleep cycle that repeats every ~90 minutes, which makes that part an ultradian rhythm.
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