BIO134

Why is Aplysia californica used as a model organism for learning and memory research?

It has a simple nervous system with only ~20,000 neurons, large identifiable neurons (making electrophysiology easy), and exhibits clear behavioral forms of learning: habituation, sensitization, and associative conditioning.

What is habituation in Aplysia, and what is its cellular mechanism?

Habituation is a decrease in the gill-withdrawal reflex after repeated non-harmful stimulation. The mechanism is increased Ca2+ channel inactivation in sensory neurons, reducing neurotransmitter release onto motor neurons.

What is dishabituation?

The restoration of a habituated response by a novel or strong stimulus. In Aplysia, a brief noxious stimulus to the tail can dishabituate the gill-withdrawal reflex.

Describe sensitization in Aplysia’s gill-withdrawal reflex.

Sensitization is an enhanced and prolonged gill-withdrawal response after a strong noxious stimulus (ex., to the tail). Facilitating interneurons release 5-HT onto sensory neuron presynaptic terminals, increasing neurotransmitter release.

What is the role of 5-HT (serotonin) in short-term sensitization in Aplysia?

5-HT released by facilitating interneurons binds to Gs-coupled receptors on sensory neuron presynaptic terminals → activates adenylyl cyclase → increases cAMP → PKA activation → 1) closes K+ channels (broadens AP), 2) enhances L-typee Ca2+ channel opening, 3) mobilizes transmitter vesicles → increased neurotransmitter release.

How does long-term sensitization differ mechanistically from short-term sensitization?

Long-term sensitization requires gene transcription and new protein synthesis. Repeated 5-HT → persistent PKA activation → CREB-1 phosphorylation (transcription factor) → gene expression → persistent kinase, ubiquitin hydrolase, growth of new synaptic connections, Short-term only modifies existing proteins.

What is a Hebbian synapse? Give the key phrase associated with it.

A synapse that strengthens when pre- and postsynaptic neurons fire together (activity-dependent plasticity). Key phrase: “Neurons that fire together, wire together.” It acts as a coincidence detector.

In Aplysia associative conditioning, what are the CS+ and US and what is the result?

The US (unconditioned stimulus) is a tail shock. The CS+ (conditioned syimulus) is a touch to the siphon or mantle. After pairing CS+ with US, touching the CS+ alone produces an enhanced gill withdrawal. CS- (unpaired) shows no enhancement.

What molecular mechanism underlies associative conditioning in Aplysia?

Activity-dependent facilitation: if CS+ activates a sensory neuron (opening Ca2+ channels) just before US-driven 5-HT arrives, the Ca2+/calmodulin greatly amplifies adenylyl cyclase activity, producing much more cAMP than 5-HT alone. The Ca2+ entry “primes” the adenylyl cyclase.

What is LTP and where is it classically studied?

Long-term potentiation (LTP) is a long-lasting increase in synaptic strength after high-frequency stimulation (50-100 Hz for ~1s). Classically studied in the CA1 region of the hippocampus, via the Schaffer collateral pathway.

What distinguishes early LTP from late LTP?

Early LTP (1 train of stimuli): lasts ~1-2 hours, involves post-translational modifications (kinase activation, AMPA receptor insertion).

Late LTP (4 trains): requires new protein synthesis and gene transcription (CREB activation), can last days to weeks.

What is the role of the NMDA receptor in LTP induction?

The NMDA receptor is a coincidence detector. It requires both 1) glutamate binding AND 2) postsynaptic depolarization (to relieve the Mg2+ block). When both occur simultaneously, Ca2+ flows in, activating Ca2+/calmodulin kinase, PKC, and tyrosine kinase → LTP.

How do AMPA and NMDA receptors differ in ion permeability?

AMPA receptors pass Na+ and K+ (not Ca2+ in most neurons) and operate at normal resting potential. NMDA receptors pass Na+, K+, AND Ca2+, but are blocked by Mg2+ at rest - block removed only by depolarization.

How does GABA’s role change between low and high frequency stimulation relevant to LTP?

At low frequency: GABA auto-inhibits its own release via presynaptic GABA-B receptors, allowing temporal summation and NMDA unblocking → LTP.

What is LTD and what frequency of stimulation produces it in CA1?

Long-term depression (LTD) is a long-lasting decrease in synaptic strength. In CA1, 1 Hz for ~15 minutes produces LTD. Mechanism: modest Ca2+ rise activates protein phosphatases → AMPA receptor dephosphorylation and internalization via clathrin-coated vesicles.

How does cerebellar LTD (Purkinje cells) differ mechanistically from hippocampal LTD?

Cerebellar LTD: parallel fibers activate AMPA+ metabotropic glutamate receptors (mGluR) → PLC → IP3 + DAG; climbing fiber simultaneously depolarizes cell → Ca2+ entry; convergence of IP3 and Ca2+ releases ER Ca2+ → PKC activation → AMPA receptor internalization.

What is neurogenesis and what type of memory does it support?

Adult neurogenesis is the birth of new cells from stem cells (ex. in the hippocampus dentate gyrus). It supports trace memory formation (hippocampus-dependent). Blocking neurogenesis with MAM impairs trace but not delay conditioning.

Distinguish trace conditioning from delay conditioning in terms of hippocampal dependence.

Trace conditioning: a gap exists between CS offset and US onset → hippocampus-dependent (slow learning, impaired by MAM).

Delay conditioning: CS and US overlap → hippocampus-independent (fast learning, unaffected by MAM).

Name four Drosophila learning/memory mutants and their biochemical defects.

dunce (dnc): lacks phosphodiesterase II → excess cAMP

rutabaga (rut): deficient in adenylyl cyclase, unresponsive to Ca2+/calmodulin

amnesiac (amn): encodes neuropeptide, normal learning but forgets after 1 hr

turnip (tur): abnormal GTP binding, reduced PKC/PKA activity

What did the calcium/calmodulin kinase transgenic mouse experiment demonstrate?

Mice lacking Ca2+/calmodulin kinase II (CaMKII) fail to show stable LTP and have impaired spatial learning in the Morris water maze, demonstrating that CaMKII is essential for both LTP and hippocampus-dependent spatial memory.

What is the holographic model of memory storage and what is its advantage over point-to-point storage?

Memory is distributed across many neurons (like interference patterns in a hologram), rather than stored at discrete points. Advantage: damage to part of the system degrades memory quality gradually rather than erasing specifically memories — consistent with brain lesion studies.

What are the four main categories of skin mechanoreceptors and their stimulus types?

Pacinian corpuscle: vibration 5-1000 Hz

Meissner corpuscle: skin motion/texture 1 — 300 Hz

Ruffini corpuscle: skin stretch

Merkel disk: fine form and texture 0 — 100 Hz

All have myelinated axons.

What is the difference between rapidly adapting (RA) and slowly adapting (SA) mechanoreceptors?

RA receptors (Pacinian, Meissner, hair follicle) respond only at stimulus onset/offset — signal changes in stimulation. SA receptors (Ruffini, Merkel) maintain a sustained discharge — signal sustained pressure/position.

What are TRP channels and what is their role in mechanosensation?

Transient Receptor Potential channels are a large family of ion channels. In mechanosensation they can be activated by a) direct membrane deformation, b) second messenger cascades, c) extracellular matrix tethering, or d) bilayer lipid composition changes. They depolarize sensory neurons.

What gene family mediates Drosophila touch sensation in bristle receptors?

The Denerin/Epithelial Na+ channel (DEG.ENaC) superfamily, specifically 16 pickpocket (PPK) genes. These mechanically-gated Na+ channels are linked via extracellular anchors and intracellular cytoskeletal links to convert bristle deflection into ion flow.

Describe mechanosensory transduction in an insect bristle receptor.

Bristle deflection → tension on extracellular anchor/tip link → opens DEG/ENaC transduction channel at the cilium tip → K+ (from high-K+ endolymph-like compartment) enters sensory neuron → depolarization → action potentials along sensory neuron axon.

Trace the path of sound waves through the human ear.

Sound → pinna → external auditory meatus → tympanic membrane (vibrates) → malleus → incus → stapes → oval window → fluid waves in scala vestibuli → basilar membrane displacement → hair cells in organ of Corti → auditory nerve → brainstem.

How does the cochlea perform frequency analysis (tonotopy)?

The basilar membrane varies in width and stiffness along its length. High frequencies (~20,000 Hz) maximally deflect the stiff, narrow base near the stapes. Low frequencies (25-200 Hz) deflect the wide, compliant apex. Each location sends signals to auditory cortex via spatially mapped (tonotopic) pathways.

Describe the ionic basis of sound transduction in inner hair cells.

The hair cell apex is bathed in endolymph (high K+; +80 mV). Hair cell interior is ~-45 mV. Sound deflects stereocilia → tip links pull open mechanically gated channels → K+ flows in (down electrochemical gradient) → depolarization → Ca2+ channels open (basolateral) → transmitter release → auditory nerve AP.

What is the tip link in hair cells and what is its proposed molecular identity?

Tip links are fine extracellular filaments connecting the tip of shorter stereocilia to the side of taller adjacent ones. They apply tension to the mechanotransduction (MET) channel (now identified as TMC1/TMC2). Deflection stretches tip links → opens MET channels.

How does the brain localize sound in space for frequencies below 2 kHz?

Inter-aural Time Difference (ITD): sound reaching one ear first generates an AP that travels to the Medial Superior Olive (MSO). MSO neurons act as coincidence detectors - they fire maximally when inputs from both ears arrive simultaneously, encoding the ITD and thus sound direction.

How is sound localization achieved for high-frequency sounds (>3 kHz)?

Inter-aural Intensity Difference (IID): the head shadows the far ear, creating an intensity difference. This is processed in the Lateral Superior Olive (LSO). High frequencies have short wavelengths so the head creates significant acoustic foreshadowing.

What is the putative ion channel complex for Merkel cell (SAI-LTMR) touch transduction?

ASIC2/ASIC3/TRPV4/Piezo 2. The Piezo2 channel in particular has emerged as a major mechanosensitive channel for light touch detection in Merkel cell-neurite complexes.

What are the five basic taste modalities?

Salty, sour, bitter, sweet, and umami (savory/amino acid taste). Each is transduced by distinct receptor mechanisms in taste receptor cells within taste buds.

What is the cellular mechanism for detecting salty taste?

Salt (NaCl) → Na+ enters taste cells through amiloride-sensitive Na+ channels (ENaC) → depolarization → transmitter release. Directly gated; no second messenger needed.

What is the cellular mechanism for detecting sour taste?

Acids (H+) block K+ channels or enter through H+ sensitive TRP channels (PKD variants) → depolarization. Also H+ can directly enter and depolarize the cell.

How are sweet and umami tastes transduced?

Sweet: T1R2+T1R3 heterodimeric G-protein coupled receptors → Gα-gustducin → PLC-β2 → IP3 + DAG → Ca2+ release → TRPM5 channel opens → depolarization.

Umami: T1R1 + T1R2 + taste mGluR4 receptors → same downstream pathway.

How is bitter taste transduced?

~30 T2R genes encode bitter receptors (multiple T2Rs expressed per taste cell → broad bitter detection). T2R → Gα-gustducin → PLC-β2 → IP3 → Ca2+ → TRPM5 → depolarization. Also α-gustducin can activate phospholipase to decrease cAMP.

What is gustducin and what is its significance?

Gustducin is a taste-specific G-protein (α-subunit) expressed in taste-receptor cells. It couples bitter (and some sweet/umami) receptors to the downstream signaling cascade (PLC-β2 pathway), analogous to transducin in photoreceptors.

Describe the general anatomy of a taste bud.

Taste buds are onion-shaped clusters (~50-100 receptor cells) embedded in papillae on the tongue. Receptor cells extend microvillae through a taste pore to contact dissolved chemicals. They synapse onto gustatory afferent nerve fibers (VII, IX). Basal stem cells continuously replenish taste cells (~2 week lifespan).

What neural pathways carry taste information from the tongue?

Anterior 2/3 tongue: cranial nerve VII (facial, chorda tympani) → nucleus of the solitary tract. Posterior 1/3 tongue/circumvallate papillae: CN IX (glossopharyngeal).

Epiglottis/esophagus: CN X (vagus).

All converge on the nucleus of the solitary tract → thalamus → gustatory cortex.

What is the “labelled line” hypothesis for taste coding?

Each taste quality is carried by a dedicated population of neurons (labeled lines) — ex. all sweet-responding fibers signal sweetness regardless of firing rate. Supported by TRPM5 knockout (abolishes sweet/bitter/umami but not salt/sour) and T2R-rescue experiments.

How many odorant receptor (OR) genes do humans have, and why did this discovery win a Nobel?

Humans have ~950 functional OR genes (mouse ~1,500), making this the largest family of GPCRs (~2% of the genome). Linda Buck and Richard Axel won the 2004 Nobel for discovering this gene family and elucidating the principles of olfactory receptor organization.

Describe the molecular mechanism of olfactory transduction in olfactory sensory neurons (OSNs).

Odorant binds OR → activates Gαolf → adenylyl cyclase III → upregulated cAMP → opens cyclic nucleotide-gated (CNG) Na+/Ca2+ channels → depolarization. Ca2+ entry then opens Ca2+-gated Cl- channels (amplification). Na+/Ca2+ exchanger restores ion balance.

What is the “one receptor, one glomerulus” rule in olfaction?

Each OSN expresses ONE of the ~1,000 OR genes. All OSNs expressing the same OR (scattered throughout the olfactory epithelium) converge their axons onto 1-2 specific glomeruli in the olfactory bulb. This creates an odor map. There are ~2,000 glomeruli in the rat.

What is combinatorial coding in the olfactory system?

Each odorant molecule activates a unique combination of ORs (and thus a unique pattern of glomeruli). Conversely, each OR responds to multiple odorants. The identity of a smell is encoded by the pattern of activated receptors across the population, not by ant single receptor.

What is the vomeronasal organ (VNO) and how does it differ from the main olfactory epithelium?

VNO is a separate chemosensory organ that expresses V1R and V2R receptors (distinct GPCR families). V1Rs mainly respond to pheromones (con-specific signals); V2Rs to kairomones (cross-species signals). VNO uses IP3/DAG (not cAMP) signaling and projects to the accessory olfactory bulb, not the main OB.

Where in the olfactory receptor neuron are receptor potentials generated, and how was this demonstrated?

Receptor potentials are generated in the cilia (where OR proteins and signaling components are concentrated). Demonstrated by applying odorant to the cilia (large receptor potential) vs. the soma (tiny response). The cilia are the transduction site.

How does the olfactory bulb process olfactory information (glomerular organization)?

OSN axons → glomeruli in olfactory bulb → synapse on mitral cell and tufted cell dendrites. Periglomerular cells provide lateral inhibition between glomeruli. Mitral cells project via the lateral olfactory tract to piriform cortex and amygdala. Different odorants activate spatiotemporal patterns of glomerular activity.

What is the fundamental claim about the visual world we perceive?

Our rich, colorful, 3D visual world full of objects is a perceptual construct - not a direct representation of physical reality.

What is the actual physical input to the visual system?

A 2D pattern of light varying in intensity and wavelength. Some species can also detect polarization of light.

Why don’t we perceive the world as jiggling as our eyes move?

The visual system actively stabilizes perception. Our eyes move in rapid jerks that are not consciously perceived.

Colors are perceptions, not physical attributes. What does light actually vary in?

Light varies in intensity, wavelength, and polarization. Colors are subjective perceptions created by the visual system.

What is the visual spectrum, and what defines it?

A narrow range of electromagnetic radiation (~400-700 nm wavelength) defined by the properties of the human eye, not by physics.

How many rods and cones are in the human retina?

Approximately 100 million rods and 3 million cones, plus ~100 million other retinal neurons. Only ~3 million axons exit via the optic nerve (convergence).

What are the key differences between rods and cones?

Rods: B/W, slow (300ms), high sensitivity, saturable, low acuity.

Cones: color, fast, low sensitivity, non-saturable, directionally sensitive, high acuity.

What is rhodopsin and what triggers its activation?

Rhodopsin is the visual pigment in rods made from opsin protein + retinal (derived from vitamin A/beta-carotene). Light causes 11-cis retinal to isomerize to all-trans retinal, activating it.

Describe the phototransduction cascade triggered by a single photon.

Light → rhodopsin activates transducin (G-protein, 70-500x amplification) → activates PDE → breaks down cGMP (4200/s) → cGMP-gated Na+ channels close → reduced dark current → ~1mV hyperpolarization. One photon closes ~200 channels (2%).

What is the ‘dark current’ in photoreceptors?

In darkness, cGMP keeps Na+ channels open in the outer segment, producing a continuous inward Na+ current (dark current). Light reduces cGMP, closing channels and hyperpolarizing the cell.

How does the photoreceptor adapt to sustained light?

Decreased Ca2+ (from closed channels) activates guanylate cyclase to restore cGMP; rhodopsin kinase phosphorylates rhodopsin increasing arresting binding; Ca2+ decrease also raises channel affinity for cGMP. All three mechanisms restore sensitivity.

What are the three types of human cone opsins and their peak sensitivities?

Short-wavelength (blue, ~419 nm), Middle-wavelength (green, ~531 nm), Long-wavelength (red, ~559 nm). Together they enable trichromatic color vision.

How have opsins evolved over time?

Opsins evolved over 630 million years. Blue pigment arose from rhodopsin first; then a single long-wavelength pigment appeared; this duplicated and diverged into red and green ~30 million years ago.

What are on-center and off-center retinal ganglion cells?

On-center cells: excited by light in center, inhibited by light in surround.

Off-center cells: inhibited by center light, excited by surround light.

Both detect contrast and spatial edges, not diffuse illumination.

How do horizontal cells create the center-surround receptive field?

Light on surround cones hyperpolarizes horizontal cells → reduces GABA release onto center cone → depolarizes center cone (disinhibition). This creates antagonistic surround via a GABA-mediated feedback loop.

What are on-center vs off-center bipolar cells and their receptor types?

On-center bipolars use inhibitory mGlu6R (depolarize in light). Off-center bipolars use excitatory AMPA-type GluR (depolarize in dark). Both driven by the same cone hyperpolarization signal.

What are the Magnocellular (M) and Parvocellular (P) pathways?

M-cells: large dendritic fields, respond transiently to large targets → overall form and motion detection.

P-cells: small dendritic fields, sustained response to small targets → fine detail and color analysis.

Describe the pathway from retina to primary visual cortex.

Retinal ganglion cells → optic nerve → optic chiasm (nasal fibers cross) → optic tract → lateral geniculate nucleus (LGN, in thalamus) → optic radiations → primary visual cortex (V1/Area 17).

What is the optic chiasm and what decussation occurs there?

The optic chiasm is where optic nerves from both eyes meet. Nasal hemiretina fibers cross to the contralateral side; temporal hemiretina fibers remain ipsilateral. Each hemisphere receives input from the opposite visual field.

How is the LGN organized into layers?

The LGN has 6 layers: layers 1 & 2 are magnocellular (M-pathway); layers 3-6 are parvocellular (P-pathway). Ipsilateral eye inputs layers 2,3,5; contralateral eye inputs 1,4,6. Interlaminar K-cells also project to V1.

What are ocular dominance columns and orientation columns in V1?

Ocular dominance columns: adjacent ~0.5mm strips of cortex preferring left or right eye input. Orientation columns: cells in a vertical column share a preferred stimulus orientation. Together they tile the cortex in a pinwheel pattern.

How are V1 layers functionally organized?

Layer 4C receives LGN input (monocular, on/off center-surround). Layers 3,4,6 contain simple cells (elongate RFs, binocular). Layers 2,3,5 contain complex cells. Layers 2/3 project to extrastriate areas (V2, V3, V4, MT).

What defines a ‘simple cell’ in V1, and how is its receptive field formed?

Simple cells have elongate, oriented receptive fields with distinct on/off subregions. Their RFs form by convergence of aligned on-center LGN geniculate cells onto layer 4C stellate cells and then to simple cortical cells.

What defines a ‘complex cell’ in V1?

Complex cells respond to oriented edges anywhere within their receptive field (position-invariant). They are direction selective and binocular. Their RFs likely arise from convergence of multiple simple cells with the same orientation but different positions.

What is an ‘end-stopped’ (hypercomplex) cell?

End-stopped cells respond best to a line of specfic length. They are inhibited when the line extends beyond the activating zone into end-zones. They arise from convergence of complex cells with inhibitory input from flanking regions.

What are color opponent cells in the retina and LGN?

Cells with spectrally opponent receptive fields: concentric single-opponent (ex. R+ center/G-surround) encode both color and brightness; co-extensive single-opponent (ex. B+/G-,R- throughout) are purely chromatic — poor spatial but good color discriminators.

Describe how binocular simple cells in V1 can encode depth (stereopsis).

Simple cells receive input from both eyes with matching orientation but slight positional offset (disparity) between left and right eye RFs. The optimal disparity for maximal response encodes depth relative to the fixation plane.

What visual illusions demonstrate that form, color, and motion are processed separately?

Motion can be perceived where there is none (motion illusions from static patterns). Objects are recognized without color (B/W processing is sufficient). The Thatcher effect shows faces processed upright-specifically for feature integration.

Why do the horizontal lines in the cafe wall illusion appear to slope?

The staggered black-and-white squares create local orientation signals at the mortar lines that bias the perceived angle. The visual system interprets local edge orientations as global line tilt.

Why does the gray haze appear to shrink when you stare at the black dot?

Neural adaptation: retinal/cortical cells responding to the gray gradient become fatigued, reducing their response over time. The perceptual fading is called Troxler’s fading or filling-in — static low-contrast signals disappear from awareness.

What is the retinotopic organization of visual projections?

Projections are organized according to position in the visual field — superior retinal quadrants (inferior visual field) run dorsally, inferior retinal quadrants (superior visual field) run via Meyer’s loop.

What is Meyer’s loop?

A bundle of fibers from the lateral geniculate nucleus that swings anteriorly around the lateral ventricle before reaching V1 — carries inferior retinal (superior visual field) information.

What are the three parallel retinal ganglion cell types projecting to the LGN?

M cells (magnocellular — large, 5%, transient, fast), P cells (parvocellular — small, 55%, sustained, wavelength-sensitive), K-cell (koniocellular — small, 40%, wavelength-sensitive).

What layers of the LGN receive M vs. P cell input?

M cells → magnocellular layers 1-2. P cells → parvocellular layers 3-6. K (koniocellular) cells → interlaminar layers between each main layer.

Where do M and P pathways terminate within V1 layer 4?

M cells → layer 4Cα.

P cells → layer 4A and 4Cβ.

K cells → blobs in layers 2/3.

How does a photoreceptor respond to diffuse light vs. simple cortical cells?

Photoreceptors respond well to diffuse light. Ganglion/geniculate cells respond moderately. Simple and complex cortical cells are ineffective with diffuse light — they need oriented bars or edges.

What is the best stimulus for a simple cell in V1?

A narrow oriented bar or edge at a specific position and orientation within the receptive field. Simple cells are found in layers 4 and 6.

What is the best stimulus for a complex cell?

An oriented bar or edge anywhere within a larger receptive field — position-invariant. Complex cells respond to orientation and movement; diffuse light is ineffective.

What is an end-stopped (hypercomplex) cell and what drives it?

A cell that responds best to a line or edge of limited length that stopes within its receptive field — corners and angles. Longer lines extend into inhibitory end-zones and suppress firing.

How do simple cells arise from LGN inputs (Hubel & Wiesel model)?

Multiple geniculate center-surround receptive fields aligned in a row converge onto stellate cells in layer 4C, which project to a simple cortical cell — the aligned arrangement creates orientation selectivity.

How do complex cells arise (circuit model)?

Multiple simple cells with the same orientation preference but offset positions converge onto a complex cell — giving orientation selectivity but position invariance.

What is orientation selectivity and how is it organized V1?

Each neuron fires maximally to one preferred bar orientation. Neurons with the same orientation preference are grouped in vertical orientation columns; preference shifts systematically across the cortex.

What are ‘blobs’ in V1?

Cytochrome-oxidase-rich patches (~50 micrometers diameter, ~1,000 neurons each, ~4 million total) in layer 2/3. Neurons inside blobs lack orientation selectivity but are color/brightness sensitive — they receive K-cell input.

What are ocular dominance columns?

Alternating stripes of cortex (in layer 4C) dominated by input from the contralateral vs. ipsilateral eye, spanning the full width of V1.

What are the three stripe compartments of V2 and what do they process?

Thin stripes (color/brightness from blobs), thick stripes (orientation/depth from layer 4B — M pathway), pale stripes (orientation, end-stops, form from 4Cβ —P pathway).

What does visual area V4 do?

Processes color constancy — neurons respond to perceived color rather than raw wavelength. Damage to V4 destroys color perception but not wavelength discrimination.

What is processed in area MT (V5)?

Motion — direction and speed of moving stimuli. most MT neurons respond to component motion; some integrate components into ‘plaid pattern’ motion (global motion).

What is the inferior temporal (IT) cortex and what is its function?

The end of the ventral stream — contains complex form- and feature-sensitive neurons. It is the ‘what is it?’ pathway for object recognition, including face-selective cells.

What are the dorsal and ventral streams?

Dorsal stream: V1 → MT → parietal lobe — processes spatial qualities, motion, and positional relationships (‘where/how’).

Ventral stream: V1 → V4 → IT — processes high-resolution form and object identity (‘what’).

What is the completion phenomenon and what does it reveal?

When a scotoma (blind spot) falls on part of a scene, the brain ‘fills in’ the missing region using surrounding context. End-stopped cells at the border fire; cells in the gap do not — the brain interpolates.

What does decomposing an image by orientation reveal?

An image can be broken into orientation channels (vertical, horizontal, oblique). Each filter reveals the edges at one orientation — recomposing all channels reconstructs the original image.