The more eccentric from fovea, the greater the “rod intrusion”.. cones rods
The retina: The outer nuclear layer structure Components of rod and cone photoreceptors. The outer segment is a stack of disks containing light-sensitive pigment molecules. The inner segment includes the cell nucleus, and synaptic terminals housed in pockets called clefts.
Stacked disks Membrane folds (invaginations)
hv hv What determines successful pigment absorption is (i.e. the photon state). = h = h
The retina: Photoreceptor responses The probability that a photon will be absorbed depends on: Direction—photons traveling through the center of the lens are more likely to be absorbed. Frequency—photons with a frequency near the peak of a receptor’s spectral sensitivity are more likely to be absorbed. Once a photon has been absorbed, the photoreceptor has no way of distinguishing its frequency.
Transduction - the conversion of photon energy into electrochemical (neural) energy.
What happens when the pigments get photolyzed?
Chromophore (contains retinal) hv Photon aborption resulting in the conversion from 11-cis to all-trans retinal is known as photoisomerization. Note: Isomers are molecules that have the same number of atoms but different physical structures, thus different properties
DARK LIGHT Na + “dark current” Na + Light activated receptors are hyperpolarized! Turn OFF neuro- transmitter. Cyclic guanosine monophosphate (cGMP) is a 2nd messenger which is ACTIVE in dark (cis-retinal + opsin) trans- Phosphodiesterase cGMP GMP
dark current....thus NT is released in the dark.. + -
ophthalmoscopic examination - Ophthalmologist views the retina through an ophthalmoscope. He or she views the fundus.
OD (oculus dexter)- right eye fundus
OS (oculus sinister)- left eye fundus Two common symptoms of disease found in the fundus: macular degeneration: heavy pigmentation around the fovea and parafovea. Results in degeneration of cones which affect central vision (scotomas). macular degeneration: heavy pigmentation around the fovea and parafovea. Results in degeneration of cones which affect central vision (scotomas). glaucoma: “cupping” or excavation of the optic disk (nerve head) due to increases in intraocular pressure (IOP).glaucoma: “cupping” or excavation of the optic disk (nerve head) due to increases in intraocular pressure (IOP).
OD (oculus dexter)- right eye fundus blood vessels maculamacula foveafovea optic disk (blind spot) temporal hemiretinanasal hemiretina centralis parafovea
* Roman numerals indicate which of von Graef’s IX layers are shown.
This is why the terms R, G & B are misnomers.
Trichromacy based on physiological response..
Based on psychophysically-derived equations from color matching of known congenital dichromats & heterochromatic flicker photometry (HFP). These curves were later corroborated by physiological monkey recordings. Trichromacy is revealed based on behavioral response..
Spectral sensitivity curves are very similar to what can be derived physically.. & physiologically..
How do these photoreceptor events relate to bipolar activity? Properties of the first synaptic layer in the retina - the outer plexiform layer. Remember: Light “turns off” photo-receptor neurotransmitter release.
Two types of bipolars: 1. Flat bipolars (sign conserving) 2. Invaginating bipolars (sign inverting) Note: In the outer plexiform layer, you have synaptic triads. Photoreceptors synapsing with two horizontal cells and either a flat or invaginating bipolar cell.
Outer plexiform layer Inner plexiform layer
Lateral interacting cells (lateral antagonism)
LUMINANCE CONTRAST -INTENSITY DIFFERENCES Without these contrasts, the brain shuts down. CHROMATIC CONTRAST -WAVELENGTH DIFFERENCES TEMPORAL CONTRAST -TIME (EVENT) DIFFERENCES
flat bipolars invaginating bipolars PR HH BP sign conserving Excitatory NT (+) PR H H BP sign inverting Hyperpolarizations (-)
flat bipolars sign conserving hv PR HH BP NOTE: The flat bipolar hyperpolarizes because of the turning OFF of excitatory NT. ALWAYS EXCITATORY
invaginating bipolars sign inverting PR H H BP NOTE: The invaginating bipolar depolarizes be- cause special membrane properties hyperpolarize with presence of glutamate. hv ALWAYS EXCITATORY
flat bipolars sign conserving hv PR HH BP NOT (EXCITATORY) - Produces “OFF” center ganglion cell G
invaginating bipolars sign inverting PR H H BP hv G (EXCITATORY) - Produces “ON” center ganglion cell
flat bipolars invaginating bipolars PR HH BP sign conserving Depolarizations (+) PR H H BP sign inverting Hyperpolarizations (-)
Lateral inhibition (lateral antagonism)
How does lateral antagonism relate to human retina?
NOT (+) means not Horizontal NOT (-): Thus, depolarization (+) - +
Spatial antagonism in the retina (i.e., the creation of ganglion cells that are either “On” center; “OFF” surround or “OFF” center; “ON” surround) allows the retina to begin processing for LUMINANCE CONTRAST.
Synaptic Dyad - inner plexiform layer BP A G Steady response from horizontal and amacrine cell integration-produces a steady-state, tonic ganglion cell response (X-cells).
Synaptic Dyad - inner plexiform layer BP A G * *possible mechanism for transient response (self-inhibiting? delay response?) Transient response from amacrine input and feedback-produces a phasic ganglion response (Y-cells).
NOTE: More neuronal convergence with eccentricity
Neuronal convergence (spatial pooling) lowers spatial acuity. However, convergence also increases overall light sensitivity.