Source: A Brain-Mind Odyssey, UC Berkeley
Tags: retina, rods, cones, rhodopsin, GPCR cascade, colour vision, scotoma, blindsight, cochlea, basilar membrane, hair cells, vestibular system, somatosensory cortex, phantom limb, motor cortex, EEG, MRI, fMRI, PET, BOLD signal
Chapter 14 covers the visual system from photoreceptor proteins and the GPCR amplification cascade through the retinal layers, LGN, and visual cortex, including colour vision, visual field deficits (scotoma, achromatopsia, prosopagnosia), and blindsight. Chapter 15 covers hearing, from the physics of sound and the cochlea's Fourier analysis through hair cells and the auditory pathway, plus the vestibular system. Chapter 16 covers somatosensory and motor systems, including body maps, phantom limbs, mirror neurons, and the cerebellum. Chapter 17 surveys brain imaging methods (X-ray, CT, MRI, EEG, MEG, PET, fMRI) with their spatial and temporal resolution trade-offs.
Retina
A complex structure at the rear of the eyeball containing light-sensitive photoreceptor cells, several layers of nerve cells, and blood vessels. Requires substantial biochemical fuel (glucose and oxygen).
Fovea (macula)
The central region of the retina where the lens focuses incoming light. Highest density of photoreceptors, particularly cones. Best visual acuity.
Blind spot
The point where all ganglion cell axons bundle into the optic nerve and exit the eyeball. No photoreceptors here. The visual system normally fills it in, so you do not notice it.
Rods
Photoreceptor cells that are numerous, distributed throughout the retina, and sensitive to very small amounts of light. Contain rhodopsin. Do not contribute to colour perception.
Cones
Photoreceptor cells mostly concentrated at the fovea. Respond to brighter light and contribute to colour perception. Three types:
S (short wavelength): violet/blue
M (medium wavelength): green/yellow
L (long wavelength): orange/red
Rhodopsin and cone-opsin
The photoreceptor proteins. Located in the outer segments of rods (rhodopsin) and cones (cone-opsin). They absorb light and initiate the transformation of light energy into a neural signal.
Retinal
A small molecule covalently bonded to the opsin protein. The actual light-absorbing component. Derived from vitamin A (retinol), which differs from retinal by a single hydrogen atom. Beta-carotene (found in carrots, kale, spinach, sweet potatoes) is the most abundant plant precursor.
Photoisomerisation (cis to trans)
When a photon is absorbed by 11-cis retinal, it straightens into the all-trans form. This shape change forces the opsin protein to change conformation, triggering the GPCR cascade.
Rhodopsin GPCR cascade
Photon absorbed by 11-cis retinal → isomerises to all-trans → opsin shape-shifts and activates
Activated opsin binds intracellular G-protein → G-protein activates
G-protein activates cGMP-phosphodiesterase
Phosphodiesterase hydrolyses cGMP → noncyclic GMP
Decreased cGMP → ion channels close → membrane potential changes → altered NT release
Enormous amplification: 1 photon → ~100 G-proteins → ~10,000 cGMP molecules hydrolysed.
Trichromatic colour vision
Humans have 3 cone types (S, M, L). By comparing the relative stimulation of each type, the brain determines the wavelength composition of incoming light.
Tetrachromatic colour vision
Some birds have 4 cone types, enabling finer wavelength discrimination and presumably a richer experience of colour.
Anomalous colour vision
Changes in the amino-acid sequence of an opsin protein alter its light-absorbing properties. Because L and M opsin genes are on the X chromosome, anomalous colour vision is more common in males (6%) than females (0.4%).
Colour blindness (red-green)
Loss of an entire functional cone type (L or M). Reduces the ability to distinguish shades in the green-yellow-red region. About 2% of males, 0.2% of females (X-linked).
Colour blindness (blue-yellow)
Nonfunctional S cone-opsin. Very rare (<0.01%), equal prevalence in males and females (not X-linked).
Retinal achromatopsia
Complete loss of all functional cone cells. The person sees only in shades of black, white, and grey. Genetic or developmental cause.
Bipolar cells
Retinal neurons that form synapses with photoreceptors on one side and ganglion cells on the other.
Ganglion cells
Approximately 1 million in the retina. Their axons bundle to form the optic nerve. They often wait for coincidences of signals from multiple photoreceptors before firing.
Horizontal cells and amacrine cells
Interneurons in the bipolar layer that contribute to lateral integration and processing within the retina.
LGN (lateral geniculate nucleus)
A pair of structures in the thalamus (diencephalon). Left LGN receives right visual field information; right LGN receives left visual field information. Sends axons to V1.
Contralateral connectivity
The crossing over of visual information: each side of the brain processes the opposite visual field.
Visual cortex
Consists of the occipital lobes and posterior temporal lobes. Contains areas V1 through V5, all highly interconnected.
Receptive field
The specific region of visual space in which a stimulus elicits a response from a given neuron.
Scotoma
A blind spot in a specific region of visual space, caused by a lesion in V1.
Hemianopia
Complete loss of vision in one half of the visual field, from a large V1 lesion.
Cortical achromatopsia
Disruption of colour vision due to a lesion in V4. Can range from faded/washed-out colour to complete loss.
Akinetopsia (motion blindness)
Caused by a lesion in V5. The person is unaware of movement in certain regions; the world appears as a series of snapshots.
Prosopagnosia
Difficulty or inability to recognise faces, caused by a lesion in the inferior and medial temporal lobe (infero-temporal cortex, where face-selective neurons are found).
Blindsight
Patients with V1 lesions (who are cortically "blind" in certain regions) can still respond to visual stimuli without conscious awareness. They can guess the orientation of lines or detect motion at above-chance levels. Explained by the 10% of optic nerve axons that project to the superior colliculus rather than the LGN, reaching higher visual areas (V2, V4, etc.) without passing through V1.
Superior colliculus
A midbrain structure receiving about 10% of optic nerve axons. Mediates rapid, unconscious responses to visual stimuli.
Cornea, lens, and pupil focus light onto the retina
Fovea: centre of retina, highest cone density, best acuity
Rods: dim light, widely distributed, no colour
Cones: bright light, concentrated at fovea, three types for colour (S, M, L)
Retinal (from vitamin A / beta-carotene) absorbs a photon and isomerises from 11-cis to all-trans
This shape-shifts the opsin (a GPCR), triggering the intracellular cascade
Massive amplification: 1 photon → 100 G-proteins → 10,000 cGMP molecules
This is how the eye can detect extremely dim light
Photoreceptors → bipolar cells → ganglion cells → optic nerve
Horizontal cells and amacrine cells provide lateral integration
Ganglion cells wait for coincident signals before firing
90% of optic nerve axons → LGN (thalamus) → V1 (posterior occipital lobe)
10% of optic nerve axons → superior colliculus (midbrain, rapid unconscious responses)
Contralateral: left visual field → right brain, right visual field → left brain
V1 lesion → scotoma (localised blindness) or hemianopia (half-field blindness)
V4 lesion → cortical achromatopsia (colour loss)
V5 lesion → akinetopsia (motion blindness)
Infero-temporal lesion → prosopagnosia (face recognition loss)
Patients with destroyed V1 can still detect visual stimuli unconsciously
The superior colliculus pathway (10% of axons) bypasses V1 and reaches V2, V4, etc.
Demonstrates that visual processing can occur without conscious awareness
Sound (physical vs. perceptual)
Physical: variation in air pressure. Perceptual: a mental experience requiring a nervous system to interpret the pressure changes.
Loudness
Associated with the amplitude (magnitude) of pressure variation. Higher amplitude = louder.
Pitch
Associated with the frequency of pressure variation. Higher frequency = higher pitch.
Timbre
The complexity of the sound waveform. Most natural sounds are complex mixtures of frequencies. Timbre is what makes different instruments sound different playing the same note.
Human hearing range
20 to 20,000 Hz.
Speed of sound
Approximately 1,100 feet per second (335 m/s, 750 mph). Far slower than the speed of light (186,000 miles per second).
Joseph Fourier / Fourier analysis
French mathematician (1768–1830). Demonstrated that any complex waveform can be represented as a sum of simple sine waves with various frequencies and amplitudes.
Tympanic membrane (eardrum)
A tissue that vibrates when air molecules strike it. Forms the boundary between the outer and middle ear.
Ossicles
Three small interconnected bones in the middle ear: hammer (malleus), anvil (incus), and stirrup (stapes). Transfer vibrations from the eardrum to the oval window.
Cochlea
A coiled, bony structure of the inner ear (found only in mammals and marsupials; more linear in other vertebrates). Filled with fluid that vibrates when the oval window moves.
Basilar membrane
Thin tissue running the length of the cochlea. Varies in thickness (thickest near the oval window, thinnest at the far end). Different regions resonate at different frequencies, performing a mechanical Fourier analysis of incoming sound.
Hair cells (inner and outer)
Cells along the basilar membrane with bundles of cilia. As the membrane vibrates, cilia bend, initiating a neural signal. Form synapses with fibres of cranial nerve VIII (auditory nerve).
Inner hair cells: approximately 3,500 per cochlea. Send signals to the spiral ganglion and brain.
Outer hair cells: approximately 12,000 per cochlea. Contain the protein prestin, which changes cell shape with membrane potential, altering basilar membrane stiffness and sensitivity. Receive more efferent input from the brain.
Hair cell signal transduction
Cilia bend → cables tug on mechanically-gated ion channels
Channels open → K⁺ flows in (depolarisation)
Depolarisation → voltage-gated Ca²⁺ channels open
Ca²⁺ influx → vesicle fusion → NT released into synaptic cleft
NT activates postsynaptic receptors on auditory nerve (CN VIII)
If threshold reached → action potential to brain
Perception of one's own voice
Much of the sound from speaking reaches the inner ear via direct vibration of skull bones rather than through the air. The frequency composition differs between bone-conducted and air-conducted sound, which is why your recorded voice sounds different.
Auditory neural pathway
Cochlea → CN VIII → spiral ganglion → cochlear nucleus (medulla) → superior olive and lateral lemniscus (pons) → inferior colliculus (midbrain) → MGN (medial geniculate nucleus, thalamus) → A1 (primary auditory cortex, temporal lobe).
Tonotopic organisation
Like a piano keyboard: different positions on the basilar membrane respond to different frequencies. High frequencies at the base of the cochlea, low frequencies at the apex.
Decibel scale
A logarithmic scale for loudness. 0 dB is the approximate threshold of human hearing. Each 10 dB increase = 10-fold increase in sound intensity. 20 dB = 100-fold increase. Quiet room ~25 dB, normal speech ~40–50 dB, noisy restaurant ~80 dB.
Hearing loss causes
Infection of the inner ear (irreversible damage to hair cells)
Genetic anomalies (e.g. connexin-26 mutation → abnormal ion balance → congenital deafness)
Acoustic trauma (loud sounds cause excitotoxic overstimulation and hair cell death)
Cochlear implant
An electrode array surgically implanted in the inner ear. A microphone picks up sound, a frequency analyser performs a crude Fourier analysis, and the auditory nerve is electrically stimulated at spatial locations corresponding to different frequencies. Produces a partial reconstruction of incoming sound.
Vestibular system
Three semicircular canals plus the utricle and saccule, all attached to the cochlea. Detects orientation relative to gravity and acceleration. Maintains balance and coordinates movement. Normally below conscious awareness.
Otoliths
Tiny crystals of calcium carbonate suspended in fluid above vestibular hair cells. Their inertia during acceleration or orientation change contributes to bending the hair cells, generating and amplifying balance signals.
Sound is rhythmic air-pressure variation
Loudness = amplitude; pitch = frequency; timbre = waveform complexity
Human range: 20–20,000 Hz
Fourier analysis: any complex waveform is a sum of sine waves
Outer ear (pinna) → ear canal → tympanic membrane → ossicles (hammer, anvil, stirrup) → oval window → cochlea
The basilar membrane varies in thickness and performs a spatial Fourier analysis
Hair cells along the basilar membrane convert mechanical vibration into neural signals
Inner hair cells (~3,500): primary afferent pathway to the brain
Outer hair cells (~12,000): contain prestin, actively modify basilar membrane sensitivity, receive efferent input from the brain
Cochlea → CN VIII → cochlear nucleus (medulla) → pons → inferior colliculus → MGN (thalamus) → A1 (temporal lobe)
Three semicircular canals detect rotation in three dimensions
Utricle and saccule detect linear acceleration and gravity
Otoliths (calcium carbonate crystals) amplify the signal by bending hair cells through inertia
Somatosensory receptors
Mechanoreceptor cells in the skin containing mechanically-gated ion channels. Respond to touch, pressure, and poking. TRP receptors in the same area respond to temperature changes.
Dorsal-root ganglion (DRG)
Clusters of cell bodies near the spinal cord. DRG neurons have peripheral dendrites (with voltage-gated Na⁺/K⁺ channels) that carry signals from skin toward the cell body, then continue on axons into the CNS. Unusually, the action potential travels toward the cell body rather than away from it.
Receptive field (somatosensory)
The region of skin within which a physical stimulus elicits activity in a specified neuron.
Primary somatosensory cortex (S1)
Located in the anterior parietal lobe, along the postcentral gyrus (immediately behind the central sulcus). Contains a topographic map of the body. Receives signals from the contralateral side. A lesion produces loss of sensation in the corresponding body region.
Somatosensory body map (homunculus)
A cortical representation of the body's sensory surface. Key features:
Roughly arranged anatomically, but with discontinuities (e.g. genitals near feet)
Hands and lips have disproportionately large representations, reflecting their high sensitivity
Demonstrates that cortical area correlates with sensitivity, not physical size
Wilder Penfield
In the 1930s, electrically stimulated regions of cerebral cortex during brain surgery in awake patients. By listening to patients describe their experiences, he mapped the somatosensory cortex.
Two-point discrimination test
A U-shaped wire test measuring somatosensory sensitivity. Fingertips and lips can distinguish two close points; the back cannot.
Posterior somatosensory cortex (S2, S3, etc.)
Also called secondary somatosensory cortex. Contains body maps but less straightforward than S1. Lesions here produce neglect syndromes and somatosensory agnosias rather than simple loss of sensation.
Neglect syndrome
Touch sensation is intact but is ignored or unrecognised unless attention is specifically drawn to it.
Phantom limb
The continued perception of a missing (amputated) limb. Caused by the region of parietal cortex that normally received input from the limb forming new connections with adjacent regions of the body map. Touching the shoulder or cheek can evoke sensations in the phantom arm.
Ramachandran's mirror box
A box with a mirror allowing the patient to see their intact hand reflected in the position of the missing limb. Watching the reflected hand "move" the phantom can reduce phantom pain. Demonstrates the power of visual feedback on somatosensory experience.
Primary motor cortex (M1)
Located immediately anterior to the central sulcus in the frontal lobe. Contains a body map of motor neurons. When M1 neurons fire, signals travel via the spinal cord to neuromuscular junctions (NMJs), where acetylcholine triggers muscle contraction. Contralateral: right M1 controls left body. Lesion produces partial paralysis.
Supplementary motor / premotor areas
Located anterior to M1 in the frontal lobe. Active before M1 during movement planning and sequencing. Lesions cause apraxia (disorganised movement) rather than paralysis.
Apraxia
Disorders of the organisation of movement. Not paralysis, but an inability to plan and sequence movements properly.
Mirror neurons
Neurons in premotor areas that are active both when performing a movement and when observing the same movement in another person.
Cerebellum
Wraps around the brainstem. Densely packed with neurons. Involved in timing and coordination of movement. Damage impairs smooth, coordinated movement.
Anosognosia
A lack of knowledge or awareness of one's own disease or deficit. Patients may confabulate explanations for why they cannot move a paralysed limb.
Mechanoreceptors and TRP receptors in the skin detect touch, pressure, and temperature
Signals travel via DRG neurons to the CNS
S1 in the postcentral gyrus contains a topographic body map (homunculus)
Hands and lips have the largest cortical representation (highest sensitivity)
After amputation, the deprived cortical region forms connections with adjacent body-map areas
Touching the face or shoulder can evoke phantom arm sensations
Ramachandran's mirror box uses visual feedback to reduce phantom pain
M1 (precentral gyrus) → spinal cord → NMJ → muscle contraction (via acetylcholine)
Premotor and supplementary motor areas handle planning and sequencing
Cerebellum handles timing and coordination
Mirror neurons fire both when acting and when observing the same action
Brain lesion
A general term for any injury or abnormality in the brain. Causes: stroke, tumour, traumatic injury, brain disease.
Stroke
A disturbance of blood flow to the brain. Two types: blockage (clot) or haemorrhage (blood vessel breaks). An aneurysm is a weak, bulging spot that may rupture.
Phineas Gage
1848 railroad accident; an iron rod passed through his frontal lobe. He survived but exhibited major personality changes (became more impulsive and socially inappropriate). Classic case demonstrating the role of the frontal lobe in personality and social behaviour.
Parkinson's disease
Neurodegenerative condition characterised by slowness and difficulty of movement. Caused by neuronal death in the substantia nigra, which produces dopamine.
Alzheimer's disease
Characterised by massive deterioration of brain tissue, enlarged sulci, and brain shrinkage.
X-ray imaging
Uses high-energy electromagnetic radiation that penetrates solid matter. Can detect bone and large lesions. Limitations: poor soft-tissue resolution in the brain, and the radiation itself is toxic (causes gene mutations and molecular damage). Wilhelm Röntgen first described X-radiation; first Nobel Prize in Physics, 1901.
CT (computed axial tomography)
A sophisticated X-ray process that takes images from many angles and uses a computer to generate a 3D reconstruction. Still widely used but involves ionising radiation. Invasive.
MRI (magnetic resonance imaging)
Generates a 3D reconstruction of internal structures using strong magnetic fields and radio waves. Based on the physical property of nuclear spin: protons behave like tiny magnets and align in a magnetic field, with two energy states that can be flipped by applying a pulse of electromagnetic energy. Non-invasive. No known toxicity from strong magnetic fields.
Tesla and gauss
Units of magnetic field strength. 1 Tesla = 10,000 gauss. Earth's magnetic field is about 0.5 gauss (50 microtesla). Clinical MRI machines typically operate at 1.5–3 Tesla.
EEG (electroencephalography)
Measures electrical activity over large regions of the cerebral cortex via scalp electrodes. Excellent temporal resolution (milliseconds). Poor spatial resolution (signal attenuated by skull). First recorded from a human brain by Hans Berger in 1920.
Wilder Penfield (eCog)
Recorded electrical activity directly from the cerebral cortex during surgery in awake patients. Much higher spatial resolution than EEG. Developed into electrocorticography (eCog).
MEG (magnetoencephalography)
Measures magnetic fields induced by electrical currents in the brain. Less distortion than EEG because magnetic fields pass through the skull without attenuation. Requires extremely sensitive detectors (SQUIDs, superconducting quantum interference devices) and magnetic shielding. Very expensive. Good temporal and reasonable spatial resolution.
PET (positron emission tomography)
Uses short-lived radioactive isotopes that decay by emitting positrons. When a positron meets an electron, they annihilate and produce two gamma-ray photons, which detectors locate. Invasive (radioactive). Expensive (requires a cyclotron to produce isotopes).
PET radioactive isotopes
F-18 (half-life 110 min): fluorinated glucose, tracks glucose consumption/metabolism
O-15 (half-life 2 min): radioactive water, tracks blood flow/oxygen consumption
C-11 (half-life 20 min): tracks organic molecule diffusion, receptor locations and densities
Image subtraction
Subtracting a control-condition PET scan from a stimulus-condition scan to isolate brain regions specifically active during a task. Used by Posner and Raichle to map language processing in the brain.
Cyclotron
A device that accelerates charged particles to high velocities using oscillating electromagnetic fields, used to create the radioactive isotopes needed for PET. Invented by Ernest Lawrence at UC Berkeley in 1930. Lawrence received the Nobel Prize in Physics in 1939.
fMRI (functional magnetic resonance imaging)
Uses MRI technology to collect a series of images over time. Detects changes in blood oxygenation associated with neural activity. Non-invasive. The current standard for functional brain imaging.
Hemoglobin
The oxygen-carrying protein in red blood cells. Has four oxygen-binding sites. Produces different magnetic properties depending on whether oxygen is attached or detached, making it detectable by MRI.
BOLD signal (blood oxygen level dependence)
The standard fMRI measurement. More neural activity → greater influx of oxygenated haemoglobin → detectable change in local magnetic properties.
Spatial and temporal resolution comparison
EEG: poor spatial (improved by more electrodes), excellent temporal (milliseconds)
MEG: better spatial than EEG (millimetres), excellent temporal (milliseconds), very expensive
PET: good spatial (centimetres), poor temporal (minutes), invasive and expensive
fMRI: good spatial (millimetres), reasonable temporal (2–6 seconds), non-invasive, most widely used
X-ray: first method; toxic radiation, poor soft-tissue contrast
CT: 3D X-ray reconstruction; still invasive
MRI: non-invasive, based on nuclear spin in a magnetic field, excellent soft-tissue contrast
EEG: measures electrical activity, great time resolution, poor spatial resolution
MEG: measures magnetic fields, less distortion, but extremely expensive (SQUID detectors + shielding)
PET: radioactive isotopes track metabolism (F-18 glucose), blood flow (O-15 water), or receptor locations (C-11). Fuzzy, expensive, invasive. Image subtraction isolates task-specific activation.
fMRI: tracks BOLD signal (oxygenated vs. deoxygenated haemoglobin). Good spatial resolution (mm), reasonable temporal resolution (2–6 s). Non-invasive. State of the art.
Need millisecond timing? Use EEG or MEG.
Need spatial localisation? Use fMRI.
Need to map receptor densities? Use PET.
fMRI has largely replaced PET for functional studies because it is cheaper and non-invasive.
⚠️ The rhodopsin GPCR cascade is a favourite exam topic. Know each step: photon → retinal isomerises → opsin activates → G-protein → phosphodiesterase → cGMP drops → ion channels close → membrane potential changes → NT release changes. Know the amplification numbers: 1 photon → 100 G-proteins → 10,000 cGMP.
⚠️ Colour vision genetics: L and M opsin genes are on the X chromosome. Anomalous colour vision and red-green colour blindness are much more common in males. Blue-yellow colour blindness is not X-linked and equally affects both sexes.
⚠️ Know what each visual cortex lesion produces: V1 → scotoma/hemianopia, V4 → cortical achromatopsia, V5 → akinetopsia, infero-temporal → prosopagnosia.
⚠️ Blindsight: the 10% of axons going to the superior colliculus (not through LGN/V1) explain unconscious visual detection. Know this pathway.
⚠️ Inner hair cells (~3,500) are primarily afferent (send signals to the brain). Outer hair cells (~12,000) contain prestin and actively modulate basilar membrane sensitivity (receive efferent input from the brain).
⚠️ The basilar membrane performs a mechanical Fourier analysis. Thick end (near oval window) resonates at high frequencies; thin end resonates at low frequencies. This is tonotopic organisation.
⚠️ Know the auditory pathway: cochlea → CN VIII → cochlear nucleus → pons → inferior colliculus → MGN → A1.
⚠️ Phantom limbs are explained by neuroplastic reorganisation in the somatosensory cortex. The deprived area forms connections with adjacent body-map regions.
⚠️ Brain imaging resolution comparison is very likely to appear on the exam. Key contrasts: EEG/MEG = best temporal; fMRI = best spatial-temporal combination; PET = unique for receptor mapping but invasive and expensive.
⚠️ BOLD signal: increased neural activity → more oxygenated haemoglobin flows in → detectable magnetic change. This is the basis of fMRI.
⚠️ PET isotopes: F-18 tracks glucose (metabolism), O-15 tracks blood flow (oxygen), C-11 tracks organic molecules/receptor densities. All are short-lived and decay by positron emission.
Q: Describe the rhodopsin GPCR cascade, starting from photon absorption.
A: A photon is absorbed by 11-cis retinal in rhodopsin, causing it to isomerise to the all-trans form. This shape-shifts the opsin protein, activating it. The activated opsin binds and activates a G-protein, which activates cGMP-phosphodiesterase. This enzyme hydrolyses cGMP to noncyclic GMP. Decreased cGMP causes ion channels to close, altering membrane potential and neurotransmitter release. Amplification: 1 photon → ~100 G-proteins → ~10,000 cGMP molecules.
Q: Why is red-green colour blindness more common in males than females?
A: The genes for L (red) and M (green) cone-opsin proteins are on the X chromosome. Males have only one X, so a single variant gene produces colour blindness. Females need variant genes on both X chromosomes.
Q: What is blindsight, and what neural pathway explains it?
A: Blindsight is the ability to detect and respond to visual stimuli without conscious awareness, seen in patients with V1 lesions. It is explained by the 10% of optic nerve axons that project to the superior colliculus in the midbrain, bypassing the LGN and V1, and reaching higher visual areas (V2, V4, etc.).
Q: How does the basilar membrane perform a Fourier analysis of incoming sound?
A: The basilar membrane varies in thickness along its length. Different regions resonate at different frequencies, with high frequencies at the thick base (near the oval window) and low frequencies at the thin apex. This spatial separation of frequencies is a mechanical Fourier decomposition.
Q: What is the difference between inner and outer hair cells?
A: Inner hair cells (~3,500 per cochlea) are the primary sensory transducers, sending signals via the spiral ganglion to the brain. Outer hair cells (~12,000 per cochlea) contain the protein prestin, which changes cell shape to modulate basilar membrane stiffness and sensitivity. They receive more efferent (brain-to-ear) input than they send afferent signals.
Q: What is a phantom limb, and what causes it?
A: A phantom limb is the continued sensory experience of a missing (amputated) limb. It is caused by neuroplastic reorganisation: the cortical region that previously received input from the limb forms new connections with adjacent body-map regions, so stimulation of nearby areas (e.g. face, shoulder) evokes phantom sensations.
Q: Compare fMRI and PET in terms of what they measure, invasiveness, and resolution.
A: fMRI measures the BOLD signal (changes in blood oxygenation related to neural activity). It is non-invasive, with good spatial resolution (millimetres) and reasonable temporal resolution (2–6 seconds). PET uses radioactive isotopes to track glucose metabolism, blood flow, or receptor densities. It is invasive, requires a cyclotron, has good spatial resolution (centimetres) but poor temporal resolution (minutes), and is expensive.
Q: What does the BOLD signal measure, and why?
A: BOLD stands for blood oxygen level dependence. When neurons become more active, they consume more oxygen. Oxygenated haemoglobin flows in to compensate. Oxygenated and deoxygenated haemoglobin have different magnetic properties, so MRI can detect the change. Greater neural activity = greater influx of oxygenated haemoglobin = BOLD signal increase.
Q: Which brain imaging technique would you choose if you needed millisecond-level temporal resolution?
A: EEG or MEG. Both can detect changes in neural activity on a millisecond timescale. MEG has better spatial resolution than EEG but is far more expensive.
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