Vision Flashcards
Retina Mapping
- Inverted and R-L reversal
- Divided into nasal & temporal hemiretinas horizontally
- R visual field —> R nasal & L temporal
- L visual field —> L nasal & R temporal
- Divided into superior and inferior hemiretinas vertically
- Superior field —> inferior retina
- Inferior field —> superior retina
- All R visual field info goes to L optic tract & all L visual field info goes to R optic tract
How is retina info transmitted to cortex?
- Optic nerve —> partial decussation at optic chiasm —> optic tract —> lateral geniculate nucleus (thalamus) —> (Meyers or Baum’s loop) —> visual cortex (specifically layer 4 of area 17)
- *mapping is maintained in LGN and visual cortex
- In cortex, superior and inferior visual fields project to specific places
- Superior field —> inferior gyrus (lingual gyrus) via Meyer’s loop
- Inferior field —> superior gyrus (cuneus gyrus) via Baum’s loop
4 Layers of Retina
- 1- Photoreceptors (rods and cones)
- 2- Bipolar cells
- 3- Ganglion (sole output of retina)
- 4- Optic nerve
Light must pass by all other layers to get to photoreceptors first
How does phototransduction work in rods?
- Rhodopsin = G protein coupled receptors
- Light absorbed by rhodopsin —> conformation change —> retinal releases opsin —> retinal dec cGMP —> dec Na+ permeability —> change in membrane potential —> dec neuroT release
- Glutamate released in dark; stopped when light
Rods v. Cones
- Rods - more numerous; all have rhodopsin so cannot detect colors
- Subserve in dark b/c can work well under low light intensity; can fire from single photon
- None in center/fovea but rapidly increase in para-fovea area
- Cones - ea contain 3 photo pigments so can compare relative amounts to distinguish color
- Subserve in daylight b/c takes more light intensity to fire
- Cone density it highest in fovea
AMD
Age-related Macular Degeneration
central atrophy and degeneration of cones in central retina w/ age; drusin deposits; lose CENTRAL vision
Retinitis pigmentosa
-genetic; degeneration of peripheral retina epithelium an photoreceptors; lose PERIPHERAL vision
Glaucoma
inc intraocular pressure —> optic nerve damage; lose PERIPHERAL first then eventually total vision loss
Diabetic Retinopathy
narrowing or blockage of blood to eyes —> ischemia —> new vascularization all over retina + transient hemorrhages so vision loss is SPORADIC; also associated w/ macula swelling (macula edema)
How do we achieve high visual acuity?
- Inc density of photoreceptors in fovea
- Meanwhile, thinner layer of intervening retinal layers in fovea (less blockage of incoming light going to photoreceptors)
- Cortical magnification (more space in area 17 is devoted to central retina (fovea) than peripheral retina
2 Types of Cortex Visual Organization
- Ocular Dominance Columns
- 4 columns (2 right and 2 left); only get info from 1 eye; segregated
- Axons coming out of layer 4 synapse on single neuron that gets input from both L and R —> integration
- Binocular depth perception
- Orientation Column System
- All neurons w/in vertical column of 6 cortical layers have same preferred stimulus orientation (fire best when stimulus is certain orientation)
How does visual processing change beyond area 17?
- Inc complexity as you move out
- Move from small to large receptive fields
- Shift from segregation to more behavior dependent grouping
2 Streams of Visual Processing
- Occipito-parietal = where pathway (spatial representation of where objects are and how fast they are moving)
- V5 (MT) - direction in which object moves across space
- Occipito-temporal = what pathway (object discrimination)
- V4 - processing color
- Inferior temporal cortex (IT) - identifying faces or hands
Strabismus
eyes misaligned b/c problem w/ extra-ocular muscles
Anisometripia
2 eyes have unequal refractive power (1 near sighted and 1 far sighted)
