Visual Systems I
The Visual Field
The visual field is the total region of space visible to one eye when fixated straight ahead.
To test its boundaries, one can move an object (like a pencil) horizontally and vertically until it disappears from view.
Each eye’s visual field is limited by:
The nose on the nasal side (approx. 60°).
The temporal side (approx. 100°).
The brow and cheek for upper and lower limits.
Images projected onto the retina are left-right reversed compared to the actual visual field.
Visual Acuity
Visual acuity refers to the eye’s ability to distinguish two nearby points.
Dependent factors:
Density and spacing of photoreceptors.
Optical precision (refraction accuracy).
Distances on the retina are expressed in degrees of visual angle:
90° = right angle.
Moon = 0.5°.
Thumb at arm’s length ≈ 1.5°.
Fist ≈ 10°.
Snellen chart measures acuity at 20 feet:
20/20 vision corresponds to identifying a letter subtending 0.083° (5 arcminutes).
Microscopic Anatomy of the Retina
The retina transforms light energy into neural activity.
The direct information pathway:
Photoreceptors → Bipolar cells → Ganglion cellsAdditional lateral connections:
Horizontal cells: link photoreceptors and nearby bipolar cells.
Amacrine cells: connect bipolar and ganglion cells; diverse functions.
Key points:
Only rods and cones are directly light-sensitive (with rare light-sensitive ganglion cells that don’t aid perception).
Only ganglion cells send output to the brain via the optic nerve.
Only ganglion cells (and some amacrines) fire action potentials; other retinal neurons signal via graded potentials.
The Laminar Organization of the Retina
The retina’s layers are inside-out — light passes through other cells before reaching photoreceptors.
Retinal transparency prevents significant distortion.
The pigmented epithelium behind photoreceptors:
Maintains photoreceptors and photopigments.
Absorbs stray light to prevent scatter.
Retinal cell layers:
Ganglion cell layer – ganglion cell bodies.
Inner nuclear layer – bipolar, horizontal, amacrine cell bodies.
Outer nuclear layer – photoreceptor cell bodies.
Plexiform layers:
Inner plexiform – synapses among bipolar, amacrine, and ganglion cells.
Outer plexiform – connections between photoreceptors, bipolars, and horizontals.
Outer segments layer – light-sensitive part of photoreceptors embedded in pigmented epithelium.
Photoreceptor Structure
Each photoreceptor includes:
Outer segment: stacked disks containing photopigments (light-sensitive).
Inner segment, cell body, and synaptic terminal.
Types:
Rods: long outer segment, many disks, very light-sensitive (~92 million per retina).
Cones: shorter outer segment, fewer disks, ~5 million per retina.
Humans have a duplex retina:
Rods: active in scotopic (night) conditions.
Cones: active in photopic (day) conditions.
Mesopic: both active under intermediate light.
Rods share one photopigment; cones have three, each tuned to different wavelengths (basis for color vision).
Cone arrangement varies between individuals; not neatly ordered like pixels.
Regional Differences in Retinal Structure and Their Visual Consequences
Fovea:
Cone-dense region at the center of macula.
Lacks rods.
Cells above cones are displaced, forming a pit for maximum visual clarity.
Peripheral retina:
Many rods, fewer cones.
Many photoreceptors converge onto single ganglion cells → more sensitivity to dim light, less acuity.
Consequences:
High spatial acuity at fovea for detail and reading.
Poor color discrimination in periphery (fewer cones).
Peripheral sensitivity to faint light (e.g., stars visible only indirectly at night).
Central blindness under scotopic conditions (rods absent in fovea).
Rods peak sensitivity ≈ 500 nm (blue-green light), explaining night color shifts.
Streetlights and dashboard designs exploit rod vs. cone spectral sensitivities (blue-green vs. red illumination).
Phototransduction in Rods
Photoreceptors convert light into changes in membrane potential via a biochemical cascade.
Mechanism resembles G-protein-coupled receptor signaling:
Light activates a photopigment, which activates G-protein (transducin) → effector enzyme (PDE) → alters cGMP → closes ion channels.
In darkness:
Rod membrane potential ≈ -30 mV (due to Na⁺ influx through cGMP-gated channels = “dark current”).
cGMP produced by guanylyl cyclase keeps channels open.
Light exposure:
Decreases cGMP → closes Na⁺ channels → hyperpolarization.
Steps in phototransduction:
Light bleaches rhodopsin.
Activates transducin (G-protein).
Activates PDE.
PDE reduces cGMP.
Na⁺ channels close → cell hyperpolarizes.
Rhodopsin = opsin (protein) + retinal (vitamin A derivative).
Light changes retinal’s shape → activates opsin (“bleaching”).
Leads to amplified signaling — a single photon can trigger a measurable response.
Phototransduction in Cones
Similar to rods but with distinct opsins:
Short-wavelength (S) cones – peak ≈ 430 nm (“blue”).
Medium-wavelength (M) cones – peak ≈ 530 nm (“green”).
Long-wavelength (L) cones – peak ≈ 560 nm (“red”).
Each cone type overlaps in sensitivity range.
Color Perception
Color determined by relative activation of S, M, and L cones.
Supported by Young-Helmholtz trichromacy theory:
The brain compares input ratios across the three cone types.
Equal stimulation → white light perception.
Unique color mixes arise from differential cone activity.
“Opponent colors” (red-green, blue-yellow) cannot be seen simultaneously.
Color blindness results from the absence of one or more cone pigment types.
Rod-only vision (no cones) → no color perception.
Dark and Light Adaptation
Transition between cone-dominant (day) and rod-dominant (night) vision takes time (minutes to nearly an hour).
Dark adaptation mechanisms:
Pupil dilation (small contribution).
Regeneration of unbleached rhodopsin.
Retinal circuit adjustments (greater rod convergence to ganglion cells).
Overall light sensitivity can increase over a million-fold.
Light adaptation reverses these changes when re-exposed to bright light.
Calcium’s Role in Light Adaptation
cGMP-gated Na⁺ channels also allow Ca²⁺ entry.
In bright light:
Channels close → Ca²⁺ entry decreases.
Lower Ca²⁺ removes inhibition on guanylyl cyclase → more cGMP produced → channels reopen.
Effect: gradual depolarization toward -35 mV, maintaining sensitivity to relative (not absolute) light levels.
Ca²⁺ also modulates photopigment and PDE sensitivity to light.
Local Adaptation of Dark, Light, and Color
Adaptation can occur locally on a cone-by-cone basis.
Demonstration:
Fixating on a black-and-white or colored pattern fatigues specific cones.
Shifting gaze to a neutral background produces negative afterimages (reversed brightness or color).
Mechanism: cones adapted to bright (or colored) areas become less responsive; perception shifts accordingly.
These effects illustrate constant micro-adjustments maintaining contrast and color perception stability.
Retinal Processing and Output
The retina’s only output to the brain comes from ganglion cell action potentials.
Goal: to understand what information about light these ganglion cells transmit.
Historical context:
Early studies (1950s) by Keffer Hartline, Stephen Kuffler, and Horace Barlow analyzed ganglion cell firing in response to light.
Initial research used horseshoe crabs and frogs, later expanded to cats and monkeys.
Found consistent processing principles across species.
Technical challenge:
Only ganglion cells (and some amacrine cells) generate action potentials.
Other retinal neurons (photoreceptors, bipolars, horizontals) use graded potentials.
Recording graded potentials required difficult intracellular recording techniques.
Major progress made in the 1970s by John Dowling and Frank Werblin, who clarified how ganglion responses arise from horizontal and bipolar cell interactions.
The Retinal Circuit
Direct pathway: cone photoreceptor → bipolar cell → ganglion cell.
Lateral modification via:
Horizontal cells: lateral interactions in the outer plexiform layer.
Amacrine cells: lateral modulation in the inner plexiform layer.
Photoreceptors release glutamate as neurotransmitter.
Depolarized in the dark, hyperpolarized by light.
Therefore, more transmitter is released in the dark — light reduces glutamate output.
Conceptual note: darkness can be thought of as the “preferred stimulus” for photoreceptors.
Example: a shadow depolarizes a photoreceptor → increases glutamate release.
In the outer plexiform layer:
Each photoreceptor contacts both bipolar and horizontal cells.
Bipolars carry information vertically toward ganglion cells.
Horizontals carry information laterally, modulating neighboring photoreceptor and bipolar activity.
The Receptive Field
The receptive field is the area of the retina where light changes the neuron’s firing rate.
Experimentally determined by projecting small light spots while recording a neuron’s output.
Light outside the receptive field does not alter firing.
This concept applies to any visual neuron — retina or brain.
Because each retinal point corresponds to a visual field location, receptive fields can also be described in visual space.
The concept extends beyond vision:
For example, in somatosensory cortex, a receptive field is a patch of skin that elicits a response when touched.
Receptive fields thus describe stimulus specificity across sensory systems.
As processing proceeds along the visual pathway:
Receptive fields become more complex (e.g., from light spots → lines → faces).
Horace Barlow’s classic frog experiment:
Certain ganglion cells responded strongly to small, moving dark spots.
The frog’s behavioral response (snapping at “bugs”) aligned with ganglion activity → early example of linking physiology to behavior.
Bipolar Cell Receptive Fields
Bipolar cells are divided into ON and OFF types based on their response to photoreceptor glutamate.
Bipolar cell receptive fields include:
Direct photoreceptor input (receptive field center).
Indirect input via horizontal cells (receptive field surround).
Direct cone–bipolar pathway:
Light → hyperpolarizes cone → affects bipolar cells differently:
OFF bipolar cells: hyperpolarize to light (turned off).
ON bipolar cells: depolarize to light (turned on).
Mechanism:
OFF bipolars use ionotropic glutamate receptors:
Glutamate binding → Na⁺ influx → depolarization.
Light (less glutamate) → hyperpolarization.
ON bipolars use metabotropic (G-protein-coupled) glutamate receptors:
Glutamate binding → hyperpolarization.
Light (less glutamate) → depolarization.
Receptive field size:
Fovea: as few as one photoreceptor per bipolar.
Peripheral retina: thousands of photoreceptors per bipolar.
Horizontal cell involvement:
Photoreceptors → horizontal cells → neighboring photoreceptors and bipolars.
When light hyperpolarizes a photoreceptor:
It hyperpolarizes connected horizontal cells.
Horizontal cell hyperpolarization reduces inhibition on adjacent photoreceptors → they depolarize.
Result: light in the surround produces the opposite effect of light in the center.
Thus, bipolar cells have antagonistic center-surround receptive fields:
Center: direct photoreceptor input.
Surround: indirect input via horizontal cells.
Center and surround produce opposite effects on membrane potential.
Dimensions:
Receptive field diameters range:
Small (fractions of a degree) near the fovea.
Several degrees in the periphery.
These bipolar receptive fields form the foundation for ganglion cell receptive fields.
Ganglion Cell Receptive Fields
Most retinal ganglion cells have center-surround receptive fields, similar to bipolar cells.
ON-center and OFF-center ganglion cells correspond to their bipolar cell inputs.
Ganglion cells fire spontaneously, even without light.
Light changes their firing rate, not just triggers it.
ON-center ganglion cells:
Increase firing when light hits center.
Decrease firing when light hits surround.
OFF-center ganglion cells:
Increase firing when dark covers center.
Decrease firing when dark covers surround.
Light affecting both center and surround equally cancels the responses → little change in firing.
Therefore, ganglion cells primarily signal contrast differences, not uniform illumination.
Edge Detection and Contrast
When a light-dark edge moves across an OFF-center receptive field:
Uniform light or dark → baseline firing.
Dark in surround → hyperpolarization → firing decreases.
Dark moving into center → excitation → firing increases.
Entire area dark → center-surround cancel → response decreases again.
Consequence:
Ganglion cells are sensitive to edges (contrast boundaries), not to absolute brightness.
The brain reconstructs visual scenes based on these local contrasts.
Visual Illusions and Contrast Effects
Ganglion receptive field organization explains brightness illusions (e.g., Figure 9.29).
Two identical gray squares can appear different depending on their background brightness.
ON-center receptive fields on a light background experience more surround illumination → more inhibition → lower response → perceived as darker.
On a darker background → less inhibition → brighter appearance.
Perceived brightness depends on contextual contrast, not physical light level.