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32 Cards in this Set

  • Front
  • Back

Compound vs. refractive eyes

Compound eye


- great depth -> motion detection


- detect wide variety of wavelengths


- sensitivity to polarized light


- covers larger angle/range




Refractive eye


- maximizes resolving power

Cornea

- continuation of the sclera


- major refractive element in the eye (air->liquid interface): 40/60 diopters of the eye

Glaucoma

- flow in choroid blood vv. ↓


-> pressure buildup of aqueous humor (still produced)


-> dmg of photoreceptors


-> loss of peripheral vision

Accomodation

- changing the refractive power of the lens by stretching/relaxing it -> focus


- near vision: ciliary muscles contract -> lens relaxes/rounds -> highest refractive power

Presbyopia

= Age-dependent loss in ability to focus on nearby objects


(due to loss of elasticity of the lens)

Fovea

Place of highest visual acuity (surrounded by macula):


- cones w/ higher resolution predominate here


- photoreceptors are closely packed here


- other neuronal cells are pulled to the side -> less distortion

Macular degeneration

- Wet - (pigmented epithelium & photoreceptors) tissue degeneration & abnormal vv. growth


- Dry - deposition of yellowish protein & lipid aggregates = drusen

Neurons of the retina

- photoreceptor cells (rods & cones)


- bipolar cells


- horizontal cells


- amacrine cells


- ganglion cells

Photoreceptor cell

Outer segment - modified cilia; membranous disks (~1000) containing photopigments -> ↑A


Inner segment - nucleus & synthetic machinery


Synaptic terminal - NT vesicles




- cells do not divide; disks renew -> phagocytosis

Rods vs. cones

- Light detection: rods more sensitive => night (scattered light) vision - more photopigment, longer, better amplification, slower (graded integration), more convergence


- Better daylight vision in cones - faster, better spatial resolution, sensitivity to direct axial rays, less convergence (almost 1:1 w/ bipolar cells), color vision (3 types of pigment/cells)

Phototransduction

Light => rhodopsin (GPCR in discs):


11-cis-retinal -> trans-retinal


-> transducin -> binds GTP -> PDE activation


-> cGMP hydrolysis


-> cGMP-gated Na/Ca channels close


-> graded hyperpolarization --| dark current


--| NT (glutamate) release [↓ inhibition]

Termination of response to light

1) Ca-mediated feedback of cGMP metabolism


- light -> Ca levels decrease -> ↓ inhibition of:


-- rhodopsin kinase --| rhodopsin (binds arrestin)


-- guanylate cyclase -> cGMP [ADAPTATION]


2) Recycling photobleached opsin (w/ disc)


- RBP (retinal binding protein) delivers trans- retinol -> epithelial cells => retinol (VitA) =>11-cis retinal -> reused

Ganglion cells in the retina

M-type (Magnocellular) - larger receptive field, motion detection


P-type (Parvocellular) - smaller receptive field, color vision


W-type - contain melanopsin -> photosensitive; importance for circadian rhythm (SCN, pretectum) & papillary reflex; homogeneous receptive field


- otherwise: On-center; surround --| AP; Off-center; surround -> AP


-- concentric organization due to horizontal cells --| photoreceptor


-- On/Off due to Δ GluR's (excitatory [NMDA, AMPA] vs. inhibitory [Meta.])


=> CONTRAST DETECTION

Treatment of vision loss

- Stem cells/precursor therapy -> photoreceptor & lens cells


- Development of photosensitive cells (using photoswitchable molecules)


- Artificial lenses/retinas (retinitis pigmentosa, macular degeneration)

Projection of retinal ganglion cells -> brain

Optic nerve -> optic chiasm (50% cross) -> optic tract ->


- hypothalamus (SCN) - circadian rhythms


- pretectum - reflex control (pupil & lens)


- superior colliculus - head/eye orientation (aligned visual, auditory, somatic topography)


- lateral geniculate nucleus (LGN) - point-to-point projection (topographic representation)

Pupillary reflex

W ganglion cells -> pretectal area


-> Edinger-Westphal nuclei (bilateral)


-> CN III -> ciliary ganglion


-> SM of pupillary sphincter


(direct & consensual)

Retinal projections to LGN of thalamus





P-type (Parvocellular) -> layers 3-6


-> color vision, fine shape discrimination


M-type (Magnocellular) -> layers 1-2


-> movement, depth, contrast




- also awake/asleep transition

Optic chiasm

Decussation (50% = nasal ganglion axons cross)


- temporal retina: Eph B1


- optic chiasm: Ephrin B2


~ repulsive interaction in growth cone


- nasal retina: do not express B1 -> decussate

LGN -> 1° Visual Cortex

~ optic radiation


- superior path -> above calcarine sulcus


(upper retinal quadrants = lower visual field)


- Meyer's loop (via temporal lobe) -> below ~


(inferior retinal quadrants = upper visual field)

1° Visual Cortex: information flow

- vertical & horizontal info flow, 2 mm thick


input: LGN -> layer 4 -> 2/3 -> 5/6


output: 2/3 -> other cortical regions (V2-5, A18, MT), 6 -> LGN


- point-to-point projection: retina -> visual cortex


=> central symmetry image inversion

Visual deficits due to visual pathway lesions

Monocular blindness - 1 eyeball dmg/CN II


Anopsia - large visual field deficit


- Bitemporal hemianopsia


- optic chiasm compression


-> nasal retinal bilateral information loss


- Homonomous hemianopsia


- any lesion more central than optic chiasm


-> 1/2 visual field vision loss

Visual cortical cell classification

Simple cell <- specifically orientated line


Complex cell <- preferred orientation & length (receive input from multiple simple cells)


Hypercomplex cell <- orientation, location, motion in a specific direction


- consecutive convergence of visual information


- vertical organization - stimulus specificity


- horizontal organization - stimulus continuum

Ocular dominance columns

- each column receives input from one eye, next to same visual field input from the other eye


= hypercolumn (continual input transition)


- blobs of cells ~ color, not orientation specificity

Transneuronal tracing

- radiolabeled proline - used to trace projections from the visual system (inject retina -> see 1° VC)


-> visualization of ocular dominance columns

Segregation of input from eyes

~ Ephrin (8) & Eph (14) gradients: LGN -> 1° VC


-> various combinations, attractive/repulsive




- also coordinated electrical activity -> pruning (critical period): bilateral input necessary for development of ocular dominance columns




- high level of plasticity (in impairment)

Eye synchronization impairments

Strabismus - misalignment of the eyes due to lack of gaze coordination


- esotropia = convergent


- exotropia = divergent




-> amblyopia (lazy eye) -> impaired vision from one eye (brain ignores input)

Visual processing

V1 (A17)


-> Motion detection (MT) - image/eye movement


-> Depth perception (V2, V3) - binocular cells


-> color vision (V4)


- respective lesions of these areas result in


- akinetopsia = motion blindness

Monocular cues for depth perception

- previous familiarity


- relative size


- interposition


- linear perspectiveness (line convergence, etc.)


- shadows & illumination


- motion parallax

Characteristics of color vision

Constancy - based on wavelengths reflected & not absorbed (not based on illumination)




Perception - hue (cone type stimulated), brightness (amount of stimulation), saturation (how much all cone systems simulated together)




Gradation - 2M combinations of the above

Color opponent cells

Single opponent cells


Center surround organized ganglion cells -> color detection:


Red/Green, Yellow/Blue, Blue/Red, etc.




-> combine into double opponent cells (+/-) in the visual cortex

Binding problem

- recombining the extracted information after parallel processing (feature maps):


parietal cortex -> master map (cohesive perception)


- selective attention


inferior temporal lobe - complex visual ID (faces)

Higher order processing abnormalities

Aperceptive agnosia = difficulty separating figures from background




Prosopagnosia = inability to recognize faces




Synesthesia = involuntary physical experience of cross-modal linkage