Biopsychology

🎯 Learning Objectives

• Describe the divisions of the nervous system (CNS, PNS, somatic, autonomic, sympathetic, parasympathetic) and the structure/function of neurons and the reflex arc (AQA 4.2.2)
• Explain synaptic transmission, including excitation and inhibition, and the endocrine system's fight-or-flight response (AQA 4.2.2)
• Evaluate localisation of function (Broca, Wernicke, motor/somatosensory cortex) and split-brain research (Sperry 1968) (AQA 4.2.2)
• Evaluate plasticity and functional recovery after trauma (Maguire taxi drivers), and ways of studying the brain: fMRI, EEG, ERP, post-mortem (AQA 4.2.2)
• Describe and evaluate biological rhythms: circadian, infradian and ultradian; endogenous pacemakers and exogenous zeitgebers (SCN, melatonin, light) (AQA 4.2.2)

📋 Key Definitions and Core Concepts

📌 Key Points

The nervous system and neurons (AQA 4.2.2)

The nervous system divides into the central nervous system (CNS) - the brain and spinal cord (the brain coordinates higher functions: cognition, emotion, planning; the spinal cord relays messages between brain and body and controls reflexes) - and the peripheral nervous system (PNS), which relays messages to and from the CNS. The PNS splits into the somatic nervous system (voluntary control of skeletal muscles; sensory neurons carry information to the CNS, motor neurons carry commands to muscles) and the autonomic nervous system (ANS) (involuntary control of internal organs: heart rate, digestion, breathing). The ANS further divides into the sympathetic branch (arouses the body - increases heart rate, inhibits digestion, prepares for action) and the parasympathetic branch (calms the body - 'rest and digest', conserves energy). The branches are antagonistic: sympathetic dominance raises heart rate, parasympathetic dominance lowers it back.

Neurons transmit electrical and chemical signals. Structure: dendrites (receive signals from other neurons), cell body (contains the nucleus), axon (carries the impulse; wrapped in a myelin sheath for insulation, with nodes of Ranvier where the impulse 'jumps', speeding conduction) and terminal buttons (communicate with the next cell across the synapse). Types: sensory neurons (carry messages from receptors to the CNS; cell body in a dorsal root ganglion, long dendrites), relay/intermediate neurons (within the CNS, connecting sensory to motor neurons; short dendrites and axons) and motor neurons (carry messages from the CNS to effectors - muscles and glands; long axons, short dendrites). Electrical transmission is via the action potential: an all-or-nothing impulse firing down the axon when the threshold (~-55mV) is reached, with resting potential (~-70mV) maintained by the Na⁺/K⁺ pump.

The reflex arc is the basic unit of nervous action: stimulus → sensory neuron → relay neuron (in the spinal cord) → motor neuron → effector (muscle). The arc is fast and unconscious because it bypasses the brain entirely (e.g. withdrawing a hand from a hot stove), and it demonstrates the automatic, protective function of the spinal cord.

Evaluation (AO3):

• Strength - biological support: neuroimaging and lesion studies confirm the divisions (ANS arousal measured physiologically - heart rate, skin conductance) and the neuron structure is universally accepted neuroscience.
• Limitation - simplification: the textbook three-neuron reflex arc is the simplest case; most neural circuits involve interneuron networks and neuromodulation far more complex than the model suggests.
• Application: understanding the ANS underpins biofeedback therapy (controlling sympathetic arousal in anxiety) and explains stress responses measured in research.

Synaptic transmission and the endocrine system: fight-or-flight (AQA 4.2.2)

Synaptic transmission is chemical communication between neurons. Process: (1) an action potential arrives at the presynaptic terminal button, opening voltage-gated Ca²⁺ channels; (2) Ca²⁺ influx causes synaptic vesicles to fuse with the presynaptic membrane, releasing neurotransmitters into the synaptic cleft by exocytosis; (3) neurotransmitters diffuse across the cleft and bind to specific receptors on the postsynaptic membrane; (4) binding produces an excitatory postsynaptic potential (EPSP) - depolarising the membrane and increasing firing (e.g. adrenaline, glutamate) - or an inhibitory postsynaptic potential (IPSP) - hyperpolarising and decreasing firing (e.g. GABA, serotonin); (5) neurotransmitters are cleared by reuptake into the presynaptic neuron (the target of SSRI drugs, which block serotonin reuptake) or broken down by enzymes. Summation decides whether the postsynaptic neuron fires: temporal summation (rapid repeated releases from one neuron add up) and spatial summation (simultaneous releases from several neurons) must jointly exceed the threshold. Synapses are unidirectional (vesicles only on the presynaptic side, receptors only postsynaptic).

The endocrine system communicates via hormones - chemical messengers released by glands into the bloodstream, slower than neural transmission but longer-lasting. The pituitary gland ('master gland') controls other glands under hypothalamic direction; the adrenal glands release adrenaline (adrenal medulla) and cortisol (adrenal cortex); the pineal gland releases melatonin (regulating sleep); the thyroid releases thyroxine (metabolism).

Fight-or-flight response: a stressor is perceived (e.g. threat) → the hypothalamus activates the sympathetic branch of the ANS and the pituitary-adrenal (HPA) axis → the adrenal medulla releases adrenaline into the bloodstream → heart rate and blood pressure rise, breathing quickens, glucose is released for energy, digestion is inhibited, pupils dilate → the body is prepared to fight or flee. Once the threat passes, the parasympathetic branch reverses the changes ('rest and digest'). Chronic activation (ongoing stress) produces prolonged cortisol release, linked to immune suppression and cardiovascular problems - a standard application point.

Evaluation (AO3):

• Strength - drug evidence: SSRIs (blocking serotonin reuptake) and antipsychotics (blocking dopamine receptors) alter synaptic transmission and change behaviour, supporting the chemical basis of psychology.
• Strength - physiological measurement: adrenaline and cortisol are measurable in blood/saliva, and heart-rate/skin-conductance measures track ANS arousal objectively - supporting research into stress.
• Limitation - fight-or-flight oversimplified: Gray (1988) proposed freeze as a first response, and Taylor et al. (2000) argued women show tend-and-befriend (protecting offspring, seeking allies) rather than fight-or-flight - the classic account is male-biased and built on animal (rat) research.
• Limitation - reductionism: explaining behaviour purely by neurotransmitter levels ignores cognitive, social and environmental factors - a standard AO3 point for the biological approach generally (biological reductionism).

Localisation of function, language centres and split-brain research (AQA 4.2.2)

Localisation of function claims specific brain areas control specific functions (as opposed to the holistic view that the whole brain works together). Cortical areas: motor cortex (frontal lobe - voluntary movement; Penfield's 'homunculus' mapping showed body parts represented in proportion to their dexterity, not size), somatosensory cortex (parietal lobe - touch, pressure, pain from the opposite side of the body), visual centres (occipital lobe - processing from both eyes via the optic chiasm) and auditory centres (temporal lobe - sound analysis).

Language centres (usually in the left hemisphere - hemispheric lateralisation): Broca's area (left frontal lobe) controls speech production; damage causes Broca's aphasia - slow, laborious speech with comprehension intact (Broca's 1861 patient 'Tan' could say only one syllable but understood speech); Wernicke's area (left temporal lobe, adjacent to the auditory cortex) controls language comprehension; damage causes Wernicke's aphasia - fluent but meaningless speech ('word salad') with poor comprehension. Broca's and Wernicke's areas are connected by the arcuate fasciculus (Wernicke's model of language processing).

Split-brain research (Sperry 1968; Gazzaniga): patients with severe epilepsy had the corpus callosum (the bundle of fibres connecting the hemispheres) severed. Sperry presented stimuli to one visual field (which projects to the opposite hemisphere): when 'RING' was shown to the right visual field (left hemisphere), patients could name it verbally; when shown to the left visual field (right hemisphere), patients could not name it but could select the object by touch with the left hand - the right hemisphere 'understood' but could not speak. Findings support hemispheric lateralisation: the left hemisphere dominates language, the right dominates visual-motor and spatial processing.

Evaluation (AO3):

• Strength - research support for localisation: Tulving's PET scans showed episodic retrieval activates the right prefrontal cortex, semantic the left; Penfield's brain stimulation during surgery mapped motor/sensory functions; case studies (Tan, Phineas Gage) support specific-area damage producing specific deficits.
• Limitation - language is not fully localised: 98% of right-handed people have language in the left hemisphere, but the equipotentiality principle (Lashley) shows the whole cortex can substitute for damaged areas - high-level functions (learning, memory) are distributed, not localised.
• Limitation - case study generalisability: 'Tan' and split-brain patients are rare and unusual (surgery for epilepsy); findings may not generalise to normal brains, and later work (Gazzaniga) showed some split-brain patients can name left-field stimuli, weakening Sperry's clean lateralisation claim.
• Limitation - plasticity (network models): modern neuroscience (fMRI) shows functions arise from distributed networks (Wernicke's model of language processing) rather than isolated spots; plasticity (Maguire's taxi drivers) shows the cortex reorganises, challenging rigid localisation.
• Practical application: localisation guides neurosurgery (mapping before tumour removal) and stroke rehabilitation (targeting damaged areas); split-brain research informs understanding of hemispheric differences.

Plasticity, functional recovery and ways of studying the brain (AQA 4.2.2)

Plasticity (neuroplasticity) is the brain's ability to change and adapt structurally in response to experience and learning: synaptic connections form, strengthen (long-term potentiation) or wither (synaptic pruning) throughout life. Evidence: Maguire et al. (2000) - London taxi drivers (who must learn 'The Knowledge') had significantly larger posterior hippocampi than controls, and volume correlated with years of driving; Draganski et al. (2006) - learning to juggle increased grey matter in visual-motor areas within three months; Kuhn et al. (2014) - video-game playing increased hippocampal grey matter. Functional recovery after trauma (stroke, injury) works through: axonal sprouting (undamaged axons grow new connections), denervation supersensitivity (receptors become more sensitive to compensate) and recruiting homologous areas (the opposite hemisphere's equivalent area takes over, e.g. Broca's area's mirror region for speech). Recovery is faster in the first few weeks, then slows; it is aided by rehabilitation (movement therapy, electrical stimulation).

Ways of studying the brain: (1) fMRI (functional magnetic resonance imaging) - detects blood oxygenation (active areas consume more oxygen): 3D images with high spatial resolution (~1-2mm), non-invasive and no radiation - but expensive, requiring the participant to stay still, with ~5-second lag (poor temporal resolution) and indirect measurement (blood flow, not neural activity). (2) EEG (electroencephalogram) - electrodes on the scalp measure overall electrical activity in the brain: high temporal resolution (milliseconds), useful for sleep research (sleep stages, dreams) and diagnosing epilepsy - but poor spatial resolution (activity from deep structures is hard to localise) and general noise. (3) ERPs (event-related potentials) - EEG data averaged over many trials, time-locked to a specific stimulus: isolates responses to stimuli with high temporal resolution - but requires many trials and background noise must be statistically removed; used in cognitive research (attention, perception). (4) Post-mortem examination - the brain is examined after death (e.g. Broca's 'Tan', Alzheimer's plaques): allows deep-structure study impossible in vivo, historically foundational - but the person is dead (causation unclear - damage may have been pre-mortem illness) and retrospective; ethical consent issues.

Evaluation (AO3):

• Plasticity - strengths: Maguire, Draganski and Kuhn all use controlled comparisons with brain imaging - converging evidence that experience changes brain structure; practical application to stroke rehabilitation and education.
• Plasticity - limitations: Maguire's taxi drivers are a unique occupational group (generalisability limited), and correlational - differences may predate the job; plasticity research is also partly animal-based (rat studies showing synaptic change).
• fMRI - evaluation: high spatial resolution and non-invasive (strengths), but poor temporal resolution, expensive, and measures blood flow indirectly - neural activity is inferred.
• EEG/ERP - evaluation: millisecond temporal resolution (strengths), useful for sleep and epilepsy, but poor spatial resolution and, for ERPs, the need for many averaged trials; no causal claims possible from correlational imaging.
• Post-mortem - evaluation: deep-structure access and historical importance, but causation is unclear and consent raises ethics; modern imaging largely supersedes it, though it remains valuable for rare conditions.

Biological rhythms: circadian, infradian, ultradian; pacemakers and zeitgebers (AQA 4.2.2)

Biological rhythms are cyclical changes in physiology and behaviour. Circadian rhythms (~24 hours): the sleep-wake cycle, body temperature (lowest ~4am, highest ~6pm) and hormone production. Endogenous pacemakers: the suprachiasmatic nucleus (SCN) in the hypothalamus (the 'master clock', receiving light information from the eyes via the retinohypothalamic tract) directs the pineal gland to release melatonin in darkness, inducing sleepiness. Exogenous zeitgebers (external cues) entrain the rhythm: light resets the SCN daily; social cues (meal times, alarm clocks, work schedules) also entrain sleep patterns. Evidence: Siffre (1975, cave study) - spent six months in a Texan cave with no external cues; his free-running sleep-wake cycle settled at ~25 hours rather than 24, showing the endogenous clock runs slightly long and needs light to entrain; Folkard et al. (1985) - participants in an underground bunker free-ran to ~25-27 hours; Aschoff and Wever (1976) - similar findings in a bunker without clocks. Morgan (1959) - SCN-lesioned hamsters lost circadian rhythmicity, which returned when the SCN was transplanted - supporting the SCN as the master clock.

Infradian rhythms (>24 hours): the menstrual cycle (~28 days, regulated by oestrogen and progesterone; ovulation mid-cycle) and seasonal affective disorder (SAD, a yearly rhythm linked to melatonin and light). Evidence: Stern and McClintock (1998) - pheromones (released in sweat) from women at the start of their cycles shortened the cycles of women mid-cycle, and vice versa, suggesting menstrual synchrony via exogenous chemical signals; Russell et al. (1980) - similar pheromone findings. Ultradian rhythms (<24 hours): sleep stages in ~90-minute cycles (NREM stages 1-4 then REM) - Dement and Kleitman (1957) found REM sleep correlated with dreaming; and the basic rest-activity cycle (BRAC) - 90-minute cycles of alertness during the day (Kleitman).

Evaluation (AO3):

• Sleep-wake cycle - strengths: converging evidence (Siffre, Folkard, Morgan) supports the SCN as master clock and light as the key zeitgeber; practical application - shift work, jet lag and light therapy for SAD.
• Sleep-wake cycle - limitations: Siffre used himself (case study, small sample, his vision deteriorated in the cave, possibly distorting light perception); small volunteer samples in bunker studies may be unrepresentative; individual differences exist (Duffy et al. 2001: 'morning' and 'evening' people have different cycle timings), so a single 'normal' 24-hour cycle is a simplification.
• Menstrual synchrony - limitations: Yang and Schank (2006) failed to replicate synchrony findings and questioned the statistics; synchrony may be coincidence; pheromone research is difficult to replicate (confounds: diet, stress, partners).
• Methodological issues: much evidence is animal-based (hamsters, rats) - extrapolation to humans is limited; lab studies remove zeitgebers artificially, so ecological validity is low, though field cave/bunker studies are higher in realism.
• Interactionist conclusion: rhythms are endogenously controlled but exogenously entrained - exam answers reward noting that neither alone explains timing (the SCN runs ~25 hours; light entrains it to 24).

💡 Worked Example

❓ Practice Questions & Mark Schemes

🎬 Video Resources

• YouTube: AQA A-level psychology biopsychology nervous system synaptic transmission localisation circadian rhythms revision

📄 Past Papers & Exam Resources

• AQA A-Level Psychology (7182) - past papers and mark schemes (AQA website; Paper 2 biopsychology questions)
• Physics & Maths Tutor - Biopsychology topic notes, past paper questions and model answers

🔗 Further Reading & Resources

• Simply Psychology - Biological Psychology: Neurons and the Nervous System
• Simply Psychology - Biological Rhythms: Circadian, Infradian and Ultradian
• Physics & Maths Tutor - Psychology revision hub (biopsychology notes, questions by topic)
• AQA - find past papers and mark schemes for Psychology 7182

🧠 Flashcards (Spaced Repetition)

📝 Exam Questions by Topic

🎯 Target Tests (Auto-Graded)

🎓 Smart Lesson (Guided)