Sensation and Perception

Sensory thresholds and signal detection

Sensory thresholds define the boundaries of what we can detect. The absolute threshold is the minimum stimulus intensity needed for detection 50% of the time — e.g., a candle flame seen from 30 miles away on a clear dark night, or a watch ticking from 20 feet in a quiet room. The difference threshold (just noticeable difference, JND) is the smallest detectable change in stimulus intensity. Weber's law states that the JND is a constant proportion of the original stimulus: ΔI/I = k, where I is stimulus intensity and k is the Weber fraction (e.g., ~0.02 for weight discrimination, ~0.08 for brightness). Fechner's law extends this: perceived intensity grows as the logarithm of physical intensity (S = k log I). Signal detection theory (SDT) moves beyond simple thresholds by incorporating decision-making under uncertainty. In any detection task, there are four possible outcomes: hit (signal present, correctly detected), miss (signal present, not detected), false alarm (signal absent, incorrectly reported), and correct rejection (signal absent, correctly not reported). SDT separates two independent factors: sensitivity (d'), the observer's actual perceptual ability to discriminate signal from noise, and response criterion (β or c), the observer's bias toward responding 'yes' or 'no' — influenced by expectations, payoffs, and motivation. The receiver operating characteristic (ROC) curve plots hit rate against false alarm rate across different criterion values; greater area under the curve indicates better sensitivity. Subliminal perception refers to stimuli below the absolute threshold that can nonetheless influence behavior (priming effects), though the MCAT emphasizes that subliminal effects are weak and short-lived compared to supraliminal processing. Sensory adaptation — the diminished sensitivity to a constant stimulus over time (e.g., no longer noticing the pressure of your watch strap) — occurs at the receptor level and frees attentional resources for novel or changing stimuli.

Vision: eye anatomy and visual pathways

Vision begins when light enters the eye through the cornea, which provides most of the eye's refractive power. The light then passes through the pupil, whose size is regulated by the iris (sphincter pupillae constricts for parasympathetic activation, dilator pupillae expands for sympathetic activation). The lens, controlled by ciliary muscles via zonular fibers, adjusts curvature for accommodation — flattening for distant objects (relaxed ciliary muscle, taut zonules) and rounding for near objects (contracted ciliary muscle, slack zonules). The retina, a neural tissue lining the back of the eye, contains three layers of cells. Photoreceptors are deepest: rods (~120 million per eye) mediate scotopic (low-light) vision, are absent from the fovea, and contain the photopigment rhodopsin; cones (~6 million) mediate photopic (color, high-acuity) vision, are concentrated in the fovea, and come in three types (S, M, L for short, medium, long wavelengths). Light hyperpolarizes photoreceptors — uniquely, they release less neurotransmitter (glutamate) in the light because cGMP-gated Na⁺ channels close when photopigments absorb photons and activate transducin, a G-protein that stimulates phosphodiesterase to break down cGMP. Bipolar cells receive photoreceptor input; ON bipolar cells depolarize to light, OFF bipolar cells hyperpolarize. Ganglion cells, whose axons form the optic nerve, have center-surround receptive fields that enhance contrast via lateral inhibition from horizontal and amacrine cells. The visual pathway: optic nerve → optic chiasm (nasal retinal fibers decussate, temporal fibers remain ipsilateral) → optic tract → lateral geniculate nucleus (LGN) of the thalamus → optic radiations → primary visual cortex (V1, striate cortex) in the occipital lobe. The dorsal stream (where/how pathway, V1 → parietal lobe) processes motion and spatial location; the ventral stream (what pathway, V1 → temporal lobe) processes object recognition and form. Damage to the ventral stream can cause visual agnosia (inability to recognize objects despite intact vision).

Color vision theories

Two complementary theories explain color vision. The trichromatic theory (Young-Helmholtz) proposes that color perception arises from the relative activation of three cone types, each maximally sensitive to a different wavelength: S-cones (~420 nm, blue/violet), M-cones (~530 nm, green), and L-cones (~560 nm, red/yellow). Any color can be matched by mixing three primary lights (red, green, blue) in varying proportions — additive color mixing. This is why computer screens use RGB pixels. Color blindness results from missing or defective cone types: protanopia (missing L-cone, red-green confusion), deuteranopia (missing M-cone, also red-green confusion, more common), and tritanopia (missing S-cone, blue-yellow confusion, rare). The trichromatic theory explains color matching at the receptor level but cannot account for afterimages, color contrast effects, or why we cannot perceive reddish-green or bluish-yellow. The opponent-process theory (Hering) fills this gap by proposing that color information is organized into three antagonistic opponent channels downstream from the cones: red vs. green, blue vs. yellow, and black vs. white (luminance). Neurons in the LGN and V1 exhibit center-surround color opponency — a cell excited by red light in its center is inhibited by green light in its surround. This explains negative afterimages: staring at a red image fatigues the red-excited cells, so when you look at a white surface, the opponent green channel is relatively stronger, producing a green afterimage. The two theories are complementary, not competing: trichromatic processing at the cone level feeds into opponent processing at the ganglion and LGN levels. Color constancy — perceiving an object's color as stable despite changing illumination — relies on the visual system's ability to discount the illuminant by comparing reflectance across the entire scene.

Hearing: ear anatomy and auditory processing

Hearing (audition) transduces sound waves — longitudinal pressure waves characterized by frequency (pitch, Hz), amplitude (loudness, dB), and waveform complexity (timbre) — into neural signals through a chain of mechanical events in the ear. The outer ear (pinna and auditory canal) collects sound waves and funnels them to the tympanic membrane (eardrum), which vibrates in response. The middle ear is an air-filled cavity containing three ossicles — malleus (hammer), incus (anvil), and stapes (stirrup) — that amplify and transmit vibrations from the tympanic membrane to the oval window of the cochlea. This impedance-matching mechanism overcomes the resistance of fluid in the inner ear; without it, ~99.9% of sound energy would be reflected. The stapedius muscle (innervated by CN VII) and tensor tympani (CN V) contract reflexively to dampen loud sounds (acoustic reflex). The inner ear contains the cochlea, a fluid-filled, snail-shaped structure divided into three compartments: scala vestibuli, scala media (cochlear duct), and scala tympani. The organ of Corti sits on the basilar membrane within the scala media and houses hair cells — the auditory receptors. Stereocilia on hair cells are deflected by shearing forces between the tectorial membrane and basilar membrane when fluid waves travel through the cochlea. Deflection opens mechanically gated K⁺ channels (the endolymph in scala media is uniquely K⁺-rich), depolarizing the hair cell and triggering neurotransmitter release onto afferent fibers of the auditory nerve (CN VIII). Frequency encoding uses two mechanisms: place theory (different frequencies maximally displace different regions of the basilar membrane — high frequencies at the base, low frequencies at the apex; primary mechanism for frequencies above ~4000 Hz) and frequency theory (the firing rate of auditory nerve fibers matches the sound frequency, up to ~4000 Hz via the volley principle, where groups of neurons fire in rotation to encode higher frequencies collectively). The auditory pathway: CN VIII → cochlear nuclei (medulla) → superior olivary complex (sound localization via interaural time and level differences) → inferior colliculus (midbrain) → medial geniculate nucleus (thalamus) → primary auditory cortex (A1, temporal lobe, tonotopically organized). Conduction deafness involves impaired transmission through outer/middle ear (e.g., earwax, ossicle damage); sensorineural deafness involves damage to hair cells or auditory nerve (e.g., loud-noise exposure, aging).

Somatosensation: touch, pain, temperature

Somatosensation encompasses touch, proprioception, pain, and temperature — mediated by diverse receptor types in the skin, muscles, joints, and internal organs. Tactile (touch) receptors in the skin are classified by receptive field size and adaptation rate. Meissner's corpuscles (dermal papillae, glabrous skin) have small receptive fields and adapt rapidly — they encode low-frequency vibration (30-50 Hz) and texture changes during active touch (e.g., gripping). Merkel's discs (basal epidermis) have small receptive fields and adapt slowly — they encode fine spatial detail, edges, and steady pressure (e.g., reading Braille). Pacinian corpuscles (deep dermis, subcutaneous) have large receptive fields and adapt extremely rapidly — they encode high-frequency vibration (250-350 Hz) and transient deep pressure (e.g., sensing a tool's initial contact). Ruffini endings (dermis) have large receptive fields and adapt slowly — they encode skin stretch, sustained pressure, and joint position. Free nerve endings in the epidermis detect pain (nociception) and temperature (thermoreception). Two-point discrimination (minimum distance at which two points are felt as distinct) varies by body region, reflecting receptive field density: fingertips (~2 mm) vs. back (~40 mm). Pain perception (nociception) involves two fiber types: fast, myelinated Aδ fibers convey sharp, localized first pain; slow, unmyelinated C fibers convey dull, diffuse, burning second pain. The gate control theory of pain (Melzack and Wall) proposes that non-painful tactile input (Aβ fibers) can close the 'gate' in the spinal cord dorsal horn, inhibiting pain transmission to the brain — explaining why rubbing a bumped elbow helps. Descending pathways from the periaqueductal gray (PAG) release endogenous opioids (endorphins, enkephalins) that inhibit nociceptive transmission. Temperature sensation relies on TRP (transient receptor potential) channels: TRPV1 activated by heat (>43°C) and capsaicin, TRPM8 activated by cool temperatures (<25°C) and menthol. The somatosensory pathway: receptors → dorsal root ganglia → spinal cord (dorsal columns/medial lemniscus for fine touch and proprioception; spinothalamic tract for pain, temperature, and crude touch) → thalamus (VPN) → primary somatosensory cortex (S1, postcentral gyrus), organized somatotopically as the sensory homunculus. Phantom limb pain illustrates cortical reorganization — the somatosensory cortex remaps after amputation, and neighboring regions invade the deafferented area, producing pain perceived in the missing limb.

Taste and smell (gustation and olfaction)

Taste (gustation) and smell (olfaction) are chemical senses that detect molecules dissolved in saliva or airborne, respectively, and are unique among sensory modalities in that receptor cells are replaced throughout life (gustatory cells ~10 days, olfactory receptor neurons ~30-60 days). Taste begins when tastants dissolved in saliva enter taste pores on taste buds, which are clustered within papillae on the tongue (fungiform, foliate, circumvallate). Each taste bud contains ~50-100 gustatory receptor cells that synapse onto afferent fibers of cranial nerves VII (chorda tympani, anterior two-thirds), IX (posterior one-third), and X (epiglottis and pharynx). The five primary taste qualities and their transduction mechanisms: sweet (sugars, G-protein-coupled T1R2/T1R3 receptors → gustducin → IP₃ → Ca²⁺ release), umami (glutamate, T1R1/T1R3 receptor), bitter (diverse toxins, T2R family, ~30 receptor types on the same cell — bitter cells act as a general poison detector), salty (Na⁺ ions enter directly through epithelial Na⁺ channels, depolarizing the cell), and sour (H⁺ ions block K⁺ channels and may enter through acid-sensing ion channels). The labeled line model suggests each taste cell type synapses onto dedicated cranial nerve fibers. The gustatory pathway: CN VII/IX/X → nucleus of the solitary tract (medulla) → VPN of thalamus → primary gustatory cortex (insula and frontal operculum). Smell (olfaction) detects airborne odorants that dissolve in the olfactory epithelium high in the nasal cavity. Olfactory receptor neurons (ORNs) extend cilia into the mucus layer, where ~350 functional types of G-protein-coupled odorant receptors (the largest gene family in the genome) bind specific molecular features. Odorant binding activates Golf → adenylyl cyclase III → cAMP → opens cyclic nucleotide-gated (CNG) channels → Na⁺/Ca²⁺ influx → depolarization. Each ORN expresses only one type of receptor, and axons from ORNs expressing the same receptor converge onto the same glomerulus in the olfactory bulb (spatial coding). The olfactory pathway is unique: it bypasses the thalamus, projecting directly from olfactory bulb to piriform cortex, amygdala, and entorhinal cortex — explaining why smells evoke powerful emotional memories (limbic system access). Flavor perception integrates gustatory, olfactory (retronasal), and somatosensory (texture, temperature) inputs; this is why food tastes bland when you have a cold (anosmia blocks retronasal olfaction).

Vestibular sense and proprioception

Vestibular sense (equilibrioception) and proprioception (kinesthesia) provide the brain with information about body position, movement, and balance — essential for coordinated motor control and spatial orientation. The vestibular system resides in the inner ear, adjacent to the cochlea, and consists of two types of structures within the membranous labyrinth: the semicircular canals and the otolith organs. The three semicircular canals (anterior, posterior, horizontal/lateral) are oriented in mutually perpendicular planes, each filled with endolymph. At the base of each canal is an ampulla containing the crista ampullaris — a gelatinous cupula into which hair cell stereocilia project. Rotational acceleration of the head causes endolymph to lag behind (inertia), deflecting the cupula and bending stereocilia. The canals operate in push-pull pairs (left and right horizontal canals are a pair; left anterior and right posterior are a pair): head rotation excites one side and inhibits the other, encoding both direction and angular velocity of rotation. The two otolith organs — utricle (horizontal acceleration, head tilt) and saccule (vertical acceleration, gravity) — detect linear acceleration and head position relative to gravity. Hair cell stereocilia in the macula are embedded in a gelatinous otolithic membrane studded with calcium carbonate crystals (otoconia/otoliths). When the head tilts or accelerates linearly, the heavy otoconia lag and deflect the stereocilia. The vestibular pathway: hair cells → vestibular (Scarpa's) ganglion → vestibular nerve (CN VIII) → vestibular nuclei (medulla/pons) → cerebellum (flocculonodular lobe), thalamus, and cortex. Vestibular output drives the vestibulo-ocular reflex (VOR), which stabilizes gaze during head movement by producing compensatory eye movements in the opposite direction (critical for reading while walking). Proprioception is the sense of body position, movement, and effort arising from receptors in muscles, tendons, and joints. Muscle spindles (intrafusal fibers) detect muscle length and rate of stretch; Golgi tendon organs (at the muscle-tendon junction) detect muscle tension and force. Together with joint receptors and cutaneous mechanoreceptors, proprioceptive input reaches the cerebellum and somatosensory cortex via the dorsal column-medial lemniscus pathway. Alcohol intoxication impairs both vestibular and proprioceptive function — the Romberg test (stand with eyes closed) reveals ataxia as the brain struggles to integrate impaired sensory signals.

Perceptual organization and Gestalt principles

Perceptual organization is the process by which the brain groups sensory elements into coherent, meaningful wholes — the central concern of Gestalt psychology ('the whole is other than the sum of its parts'). Gestalt principles describe innate rules the visual system uses to organize ambiguous input: figure-ground relationship (we segregate a scene into a distinct figure that stands out from the background; Rubin's vase-face illusion demonstrates reversibility), proximity (elements close together are grouped), similarity (elements sharing features — color, shape, size — are grouped), continuity (the visual system prefers smooth, continuous contours over abrupt direction changes), closure (incomplete figures are perceived as complete — the brain fills missing contours), connectedness (elements connected by lines or other visual features are grouped), and common fate (elements moving together in the same direction are grouped — a flock of birds is perceived as a single unit). The law of Prägnanz (simplicity) states that perceptual organization favors the simplest, most stable interpretation. Top-down processing (conceptually driven) uses prior knowledge, expectations, and context to interpret sensory input — reading a smudged word relies on top-down expectation. Bottom-up processing (data-driven) begins with sensory receptors and builds upward to perception — detecting edges, colors, and motion from raw retinal input. Perception typically involves both working in parallel. Perceptual set is a mental predisposition to perceive one thing and not another, shaped by context, motivation, culture, and emotion. The 'rat-man' ambiguous image demonstrates: participants shown animal pictures beforehand see a rat; those shown faces see a man. Selective attention — the focused awareness of a subset of sensory input — is demonstrated by the cocktail party effect (noticing your name in an unattended conversation) and dichotic listening tasks (shadowing one ear's message while ignoring the other). Inattentional blindness (failing to notice a fully visible but unexpected object when attention is elsewhere — e.g., the gorilla in the basketball-passing video) and change blindness (failing to notice changes in a scene) illustrate the limitations of attention. Divided attention (multitasking) incurs a performance cost because attentional resources are limited.

Depth perception and perceptual constancy

Depth perception is the ability to perceive the three-dimensional world from two-dimensional retinal images, relying on both binocular and monocular cues. Binocular cues require both eyes: retinal disparity (each eye receives a slightly different image because they are ~6 cm apart; greater disparity for closer objects — the basis of stereopsis) and convergence (the inward rotation of the eyes as an object approaches; extraocular muscle proprioception signals depth). Monocular cues (pictorial depth cues) work with one eye and are exploited by artists to create the illusion of depth on a flat surface. Relative size: if two objects are assumed similar in size, the one casting a smaller retinal image is perceived as farther away. Interposition (occlusion): an object that partially blocks another is perceived as closer. Relative height: objects higher in the visual field are perceived as farther away (for objects below the horizon line). Texture gradient: texture elements appear denser and less distinct with distance. Linear perspective: parallel lines appear to converge with distance (e.g., railroad tracks). Light and shadow: the visual system assumes light comes from above; shading and cast shadows provide depth cues about shape and relative position. Motion parallax: when moving, nearby objects appear to move faster across the visual field than distant objects — a powerful monocular depth cue exploited by many animals without stereopsis (e.g., pigeons bob their heads to generate motion parallax). Perceptual constancy refers to the perception of stable object properties despite changing sensory input. Size constancy: an object's perceived size remains constant despite changes in retinal image size with distance — achieved by integrating retinal size with perceived distance (size-distance scaling). The Ames room illusion exploits this: a trapezoidal room appears rectangular from a peephole, causing equal-sized people in opposite corners to appear dramatically different in size because the visual system misapplies size constancy. Shape constancy: perceived shape remains stable despite changes in viewing angle (a door opening appears rectangular, not trapezoidal). Brightness/lightness constancy: perceived reflectance remains stable despite changes in illumination (a white shirt looks white in dim light and bright sun — it reflects a higher proportion of available light regardless of absolute luminance). Color constancy: mentioned under color vision; the same principle applied to chromatic perception. Visual illusions (Müller-Lyer, Ponzo, moon illusion) demonstrate how perceptual constancy mechanisms, when misapplied or placed in conflict with contextual cues, produce systematic errors — the MCAT frequently tests these as demonstrations that perception is constructive, not a direct recording of reality.

How it works

Sensation and perception follow a universal sequence: physical energy → transduction → neural signal → thalamic relay (except olfaction) → primary sensory cortex → higher-order processing. For each sensory modality, the MCAT expects you to know (1) the adequate stimulus (what physical energy the system detects), (2) the receptor and its transduction mechanism, (3) the pathway from receptor to cortex, and (4) how the brain organizes this input into conscious percepts. When answering P/S passage questions, identify whether the scenario describes a sensory process (bottom-up, receptor-level, threshold-based) or a perceptual process (top-down, interpretive, context-dependent). If the passage introduces a graph with hit and false alarm rates, think signal detection theory and distinguish sensitivity (d') from criterion shifts. If it shows illusions or grouping effects, think Gestalt principles or constancy mechanisms. The unifying MCAT theme: perception is not a passive recording — the brain actively constructs, interprets, and sometimes misinterprets the sensory world.

How it works

Sensation and perception follow a universal sequence: physical energy → transduction → neural signal → thalamic relay (except olfaction) → primary sensory cortex → higher-order processing. For each sensory modality, the MCAT expects you to know (1) the adequate stimulus (what physical energy the system detects), (2) the receptor and its transduction mechanism, (3) the pathway from receptor to cortex, and (4) how the brain organizes this input into conscious percepts. When answering P/S passage questions, identify whether the scenario describes a sensory process (bottom-up, receptor-level, threshold-based) or a perceptual process (top-down, interpretive, context-dependent). If the passage introduces a graph with hit and false alarm rates, think signal detection theory and distinguish sensitivity (d') from criterion shifts. If it shows illusions or grouping effects, think Gestalt principles or constancy mechanisms. The unifying MCAT theme: perception is not a passive recording — the brain actively constructs, interprets, and sometimes misinterprets the sensory world.

Comparisons

• C/P (Wave physics): Sound waves are longitudinal pressure waves; frequency = pitch, amplitude = loudness. Light is electromagnetic radiation; wavelength = color (visible spectrum ~380-750 nm), amplitude = brightness. Understand the relationship v = fλ.
• C/P (Signal detection theory): SDT is statistical decision theory applied to perception. The ROC curve plots hit rate vs. false alarm rate; d' measures signal/noise separation (detectability independent of criterion). Expect data interpretation passages with SDT outcomes.
• B/B (Phototransduction): Rhodopsin (opsin + 11-cis retinal) in rods; light isomerizes retinal to all-trans → activates transducin (Gt, a GPCR) → phosphodiesterase → cGMP decrease → Na⁺ channel closure → hyperpolarization. Cones use similar cascade with cone opsins.
• B/B (Hair cell transduction): Stereocilia deflection opens mechanically gated K⁺ channels (unique: K⁺-rich endolymph means K⁺ influx depolarizes, not hyperpolarizes). Tip links connect adjacent stereocilia; tension opens channels.
• B/B (Neuroscience): RElevant cranial nerves — CN I (olfactory), CN II (optic), CN VII (facial, taste anterior 2/3), CN VIII (vestibulocochlear), CN IX (glossopharyngeal, taste posterior 1/3), CN X (vagus, taste epiglottis).
• P/S (Neuropsychology): Visual agnosia (ventral stream lesion), prosopagnosia (fusiform face area), phantom limb (cortical reorganization), synesthesia (cross-modal perception), motion blindness/akinetopsia (dorsal stream/V5 lesion).

Common confusions

• Confusing Weber's law (ΔI/I = k, a proportion) with Fechner's law (S = k log I, a logarithmic relationship between perceived and physical intensity). Weber applies to discrimination thresholds; Fechner applies to subjective magnitude.
• Misidentifying which signal detection outcome changes when criterion shifts. A conservative criterion → fewer hits AND fewer false alarms. A liberal criterion → more hits AND more false alarms. Sensitivity (d') does NOT change when only criterion shifts.
• Thinking the trichromatic and opponent-process theories compete rather than complement. Trichromatic explains cone-level (receptor) color matching. Opponent-process explains post-receptoral (ganglion/LGN/V1) color opponency and afterimages.
• Mistaking the basilar membrane's frequency mapping (tonotopy). High frequencies displace the BASE (stiff, narrow, near oval window). Low frequencies displace the APEX (wide, floppy, far end). Remember: 'high pitch at the start, low at the far part.'
• Forgetting that olfactory information bypasses the thalamus on its initial projection to cortex. All other sensory modalities relay through the thalamus (LGN for vision, MGN for hearing, VPN for somatosensation and taste). Smell projects directly to piriform cortex. This exception is a classic MCAT discrete question.
• Confusing conduction deafness (outer/middle ear, e.g., impacted cerumen, otosclerosis) with sensorineural deafness (inner ear/CN VIII, e.g., hair cell damage from loud noise, presbycusis). Conduction: bone conduction works, air conduction impaired. Sensorineural: both impaired.

Quick review

• Absolute threshold: minimum stimulus detected 50% of the time. Difference threshold (JND): smallest detectable change. Weber: ΔI/I = k. Fechner: S = k log I.
• Signal detection: 4 outcomes — hit, miss, false alarm, correct rejection. d' = sensitivity (discriminability). β/c = criterion (bias). ROC curve: hit vs. false alarm rate.
• Vision: cornea/lens focus light onto retina. Rods (low-light, rhodopsin, none in fovea). Cones (color, high acuity, concentrated in fovea). Light hyperpolarizes photoreceptors (cGMP channel closure).
• Visual pathway: retina → optic nerve → optic chiasm (nasal decussate) → LGN (thalamus) → V1 (occipital). Dorsal stream/parietal = where/how (motion). Ventral stream/temporal = what (object recognition).
• Trichromatic theory: 3 cone types (S/blue, M/green, L/red). Explains color matching. Opponent-process: red-green, blue-yellow, black-white opponent channels explain afterimages.
• Auditory pathway: pinna → eardrum → ossicles (malleus, incus, stapes) → oval window → cochlea → hair cells on basilar membrane → CN VIII. Place theory (high freq = base) + frequency/volley theory (low freq).
• Somatosensation: Meissner (rapid, small RF), Merkel (slow, small RF), Pacinian (very rapid, large RF), Ruffini (slow, large RF). Aδ = fast sharp pain, C = slow dull pain. Gate control: touch inhibits pain.
• Taste: sweet/umami/bitter = GPCR; salty = Na⁺ channels; sour = H⁺ channels. Olfaction: GPCR → Golf → cAMP → CNG channels. Olfaction bypasses thalamus (goes directly to piriform cortex).
• Vestibular: semicircular canals (rotation), otolith organs/utricle + saccule (linear acceleration, gravity). Proprioception: muscle spindles (length), Golgi tendon organs (tension).
• Gestalt: figure-ground, proximity, similarity, continuity, closure, common fate. Top-down (concept-driven) vs. bottom-up (data-driven). Inattentional blindness, change blindness, cocktail party effect.
• Depth: binocular (retinal disparity, convergence) + monocular (relative size, interposition, relative height, texture gradient, linear perspective, light/shadow, motion parallax).
• Constancies: size (size-distance scaling), shape, brightness, color. Illusions (Müller-Lyer, Ponzo, Ames room) exploit constancy mechanisms misapplied.