Test 2 - Vision Flashcards
What do the different layers of the retina consist of?
Inside
1. Pigment epithelium
2. Outer segment of photoreceptors
3. Outer nuclear layer
4. Outer plexiform layer
5. Inner nuclear layer
6. Inner plexiform layer
7. Ganglion cell layer
Outside (light)
Pigment epithelium
protective layer not involved with vision
Outer segment of photoreceptors
where light receptors are located (rods and cones top part) - input layer
Outer plexiform layer
rods and cones are in contact with horizontal, bipolar, and amacrine cells
Outer nuclear layer
cell bodies of rods & cones (nucleus)
Inner nuclear layer
cell bodies of the horizontal, bipolar, and amacrine cells
Inner plexiform layer
where horizontal, bipolar, and amacrine cells are in contact with RGCs
Ganglion cell layer
RGCs are located here and communicate with optic nerve (output layer)
What does RGC stand for?
retinal ganglion cell
Rods
photon (bundle of light energy) detectors
Cones
visual acuity and color
What is the receptor name used in rods?
Rhodopsin
What is the name of the G-protein associated with the GPCR in rods?
Transducin
What do guanylate cyclase and phosphodiesterase do in cells, respectively?
They are both used in phototransduction (biochemical reactions triggered by photon absorption)
Dark - guanylate cyclase - converts GTP into cGMP and PDE is inactive
Light - GC converts GTP into cGMP which is cleaved by PDE into GMP
(dark=cGMP ; light=GMP)
Describe what happens in rods when light hits rhodopsin
Light:
1. light hits rhodopsin and alters conformation bringing it closer to transducin
2. activation of transducin leads to activation of effector PDE
3. PDE breakdown cGMP (2nd messenger) to GMP
4. This leads to cGMP-gate cation channels closing (CNG channels)
5. Once channels are closed the rods will be hyperpolarized (no a.p./NTs)
6. All decrease glutamate released from rod
(light stops activation of rods because it induces the destruction of the 2nd messenger)
Describe what happens in rods when light is off, meaning no light his rhodopsin.
- no light to change the conformation of rhodopsin
- cGMP remains in cell (is not cleared by PDE)
- cGMP binds to CNG channel
- CNG is a nonselective channel which allows: Na, Ca (*), K efflux
- Depolarization occurs and glutamate released
Describe the cell pathway behind recovery.
Recovery = light-activated photoreceptors return to “dark state”
- stop activating PDE
- stop cutting up cGMP
- cGMP levels increase & bind to CNG
- CNG opens and Ca comes in
- increase in Ca leads to an increase in GCAP which activates GC
- GC makes cGMP from GMP
- Na and Ca continue coming in leading to depolarization
- Arrestin activated (binds to GPCRs to deactivate them)
Describe Weber’s law as it relates to adaptation in vision
Weber’s law states that an increase in stimulus plus a lesser new stimulus you will perceive the new stimulus poorly. It must be different enough from original to be sensitive to charge
- depends on Ca concentrations
Adaptation
In vision is the adjustment of photoreceptors sensitivity according to background light level (less sen. if background bright)
- depends on Ca concentrations
Where are most cones located?
near center - fovea centralis
What is the difference between a dichromat and a trichromat when it comes to cones?
Trichromats - have 3 cone types (RGB)
Dichromats - have 2 cone types (RG)
What is meant by Chromatic Aberration? What leads to this?
Color blindness - mutation in given cones opsin gene
Do all people have the same number of each of the 3 cones? Explain.
No, there are differences in color perception from person to person - blue cones are the rarest (hardest to perceive)
Explain the difference between bipolar ON cells and bipolar OFF cells.
bipolar ON - metabotropic glutamate receptors (cell depolarized with light)
bipolar OFF - ionotropic glutamate receptors (cell hyperpolarized with light)
Explain how bipolar ON cells communicate when light hits a cone
- light on leads to hyper polarization of cones and less glutamate release
- metabotropic receptors less active
- inhibitory G proteins are less active
- cation channels are less inhibited
- on bipolar cell depolarized
- light keeps ON bipolar on
Explain how bipolar OFF cells communicate when light hits a cone
- light on leads to hyper polarization of cones and less glutamate release
- ionotropic receptors less active
- fewer cations enter bipolar cell
- OFF bipolar cell is hyperpolarized
- light keeps OFF bipolar cells OFF
What does a horizontal cell do?
its job is lateral inhibition and is contact with all three cones
If you have a green, a blue, and a red cone, and the green cone is the one perceiving green wavelengths of light, what does the horizontal cell do? (explain the whole process before the horizontal cell too)
The green cone receives the green wavelength. The opsin receptor changes conformation and activates PDE so that we destroy cGMP and close the CNG channel- this stops calcium from coming in. We hyperpolarize this cone and stop sending glutamate. ON Bipolar cells with metabotropic receptors will switch on in this instance while OFF Bipolar cells with ionotropic receptors will be off without glutamate. Since the blue and red cones are not receiving any light of their wavelengths, they are going to be depolarized and send glutamate to horizontal cells, which send GABA back to all 3 of the cones. This further inhibits the activity of the green cone (strengthening the signaling of the ON Bipolar connected to the green cone).
Describe the tract of visual information in the brain.
- eye
- optic nerve
- optic chiasm
- optic tract
- suprachiasmatic nucleus (stop)
- lateral genticulate nucleus (stop)
- superior colliculus (stop)
- primary visual cortex (V1)
Suprachiasmatic nucleus of the hypothalamus
hormonal and metabolism regulated by light input
Lateral geniculate nucleus
stops here before V1
Superior colliculus
integrates visual info
What is the difference between P and M pathways for visual processing?
M pathway -> superior colliculus -> V1 = colorblind/fast (certain RGCs for light movement not color)
P pathway -> superior colliculus -> V1 = acuity & color (less motion based & more focused)
What is the difference between ventral and dorsal streams?
Ventral = “what” stream - leads to the temporal cortex - which analyzes form and color
Dorsal = “where” stream - leads to the parietal cortex - analyzes motion and depth
What part of the brain is primarily responsible for your cognition of vision and ability to infer information?
prefrontal cortex to hippocampus
What is the brain region associated with facial recognition?
Fusiform face area (6 patches)
Middle patch (ML, MF)
view faces most specific for specific angles and peripheral vision
Anterior-lateral patch (AL)
specific angles, recognize mirror image of face
Anterior medial (AM)
faces from all views
What is the LIP?
lateral intraparietal area
(The LIP analyzes info. from the MT (neurons sensitive to direction of motion))
What is interesting regarding the LIP when discussing consciousness?
It send information from frontal cortex to regions that control eye movement - Sleep-wake cycles shut off in anesthetized animals, active in wake/REM
Chemoaffinity
how well attraction to chemical cue/recognition of extracellular molecular cues on neuronal growth cone receptors
Chemoattraction
attractive cues - like molecules
Chemorepulsion
repulsive cues - doesn’t like molecules
Where are the two places where chemical cues can be located for chemoaffinity?
- cell surface bound
- secreted (at a distance)
- If RGC axons show a gradient for EphA receptor expression temporal>medial and the superior colliculus shows an Ephrin A ligand expression gradient of anterior > posterior, where will a temporal RGC axon land when it gets to the superior colliculus, anterior or posterior?
anterior
temporal axons -> anterior tectum (express increase amounts of EphA receptors)
nasal axons -> posterior tectum (decrease ion levels)
What is axon competition?
axons not wanting to end up in the same space - and solves the event where axons aren’t repelled by a repellant for which they have a receptor - filling of target space repels another axon
How do chemorepellants and chemoattractants change the direction of the growth cone of an axon?
Growth cone signaling is dependent on actin polymerization
