Week 2 - Retinal Phototransduction and Signal Processing Flashcards

1
Q

sclera

  • what is it?
  • what does it do?
A

relatively spherical and avascular, white dense connective tissue that covers globe posterior to cornea

  • provides strong tough external framework to protect delicate optic and neural structures
  • maintains shape of globe so retinal image is undisturbed and provides attachment for extraocular muscles to rotate globe and ciliary muscle to accommodate lens
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2
Q

cornea

  • what is it?
  • what does it do?
A

“window of the eye”

  • mechanically strong and transparent connective tissue that covers anterior 1/6 of eye
  • most powerful focusing element of the eye, roughly twice as powerful as lens
  • responsible for 80% of refraction in eye
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3
Q

lens

  • what is it?
  • what does it do?
  • what does it contain?
A

specialized epithelial tissue that is responsible for fine-tuning image that is projected on retina

  • lies inside eye surrounded by aqueous humor
  • transparent and has high refractive power
  • elastin-based zonular fibrils stabilize lens and allow accommodation to occur
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4
Q

what is the uveal tract made of?

A

consists of 3 structures

  • choroid
  • ciliary body
  • iris
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5
Q

choroid

A

capillary bed nourishing photoreceptors and outer retina

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6
Q

ciliary body

A

has two parts:

  • ciliary muscle: controls refractive power of lens
  • vascular component: produces aqueous humor filling anterior chamber
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7
Q

iris

A

colored part of eye seen through cornea
-has 2 sets of muscles with opposing actions that allow size of pupil (opening at center) to be adjusted by neural control

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8
Q

anterior chamber

A

volume behind cornea and in front of lens

-filled with aqueous humor

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9
Q

posterior chamber

A

region between vitreous and lens

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10
Q

aqueous humor

-production and flow

A

clear watery liquid that nourishes cornea and lens

  • produced by vascular component of ciliary body/epithelium lining ciliary processes
  • flows around lens and through pupil into anterior chamber
  • leaves eye by passive flow at anterior chamber angle
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11
Q

vitreous humor

A

thick gelatinous substance filling space between back of lens and surface of retina

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12
Q

retina

A

contains neurons that absorb light and process visual info in images and send that info to the brain

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13
Q

macula

A

oval spot containing a yellow pigment (xantophyl)

-supports high acuity

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14
Q

fovea

  • what makes it special?
  • what is the visual angle?
A

small depression at center of macula

  • has highest spatial acuity by pushing away ganglion cells, IPL, and INL
  • visual angle subtended is 0.5 degrees (full moon or thumb nail at arm distance)
  • involves 0.01% of retinal area, but 10-50% of optic nerve
  • no S cones or rods
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15
Q

optic disk

A

whitish circular area where retinal axons leave eye and travel through optic nerve to targets in midbrain and thalamus
-site where blood vessels supply inner retina enter eye

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16
Q

blood supply of eye

A

ocular vessels are derived from ophthalmic artery (from internal carotid) divides into 2 vascular systems

  • anterior segment = iris and ciliary body
  • retinal systems
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17
Q

vascularization of anterior segment

A

originates from anterior ciliary arteries and long posterior ciliary arteries
-penetrating vessels through sclera vascularize iris and ciliary body

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18
Q

retinal blood supply

A

delivery of metabolic substrates and O2 to retina is accomplished by two separate vascular systems: inner retinal and choroidal
-retinal and choroidal vessels differ morphologically and functionally from each other

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19
Q

cataracts

  • what it is
  • risk factors
  • symptoms
  • treatment
A

clouding of lens that affects vision, mostly related to aging, and leading cause of blindness worldwide (50% Americans have/had cataracts by 80 yo.)

  • RF: aging, diabetes, sunlight, smoking
  • symptoms: hazy vision, poor night vision, glare, faded colors
  • treatment: surgical removal of cloudy lens, replacement with artificial lens; very little recovery time required after surgery
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20
Q

how are cataracts formed?

A

disruption in order of organization of lens cell fibers, or aggregation of PRO within them, can destroy transparency of cell

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21
Q

glaucoma

  • what it is
  • risk factors
  • symptoms
  • treatment
A

group of diseases that damage eye’s optic nerve and result in loss of peripheral vision fields

  • RF: elevated eye pressure (from poor drainage of aqueous humor), thin cornea, abnormal optic nerve anatomy, HTN
  • symptoms: none until too late (loss of peripheral visual fields)
  • TRT: eye drops to decrease aqueous production and/or increase drainage
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22
Q

types of glaucoma

A
  1. normal tension
  2. open angle
  3. closed angle
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23
Q

difference between open and close angle glaucoma

A

open: slow development of pathology
- caused by obstruction of drainage canals
close: sudden increase in intraocular pressure due to collapse of wall blocking drainage (more severe)
- closed or narrow angle between iris and cornea

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24
Q

where to photoreceptors point?

A

towards the back of the eye

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25
Q

how does light enter the eye?

A

light comes in first hitting the ganglion cell layer, the rest of the inner retina, then photoreceptor (PR) nuclei and inner segments before PR outer segments where phototransduction occurs

  • thus light must travel through thickness of retina before striking and activating rods and cones, so absorption of photons by visual pigment of photoreceptors is translated into first biochemical message into electrical message that can stimulate all succeeding neurons of retina
  • -retinal message concerning photic input is transmitted to brain by spiking discharge pattern of ganglion cells via optic nerve
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26
Q

what are the 7 layers of the retina? what kind of cells do they have?

A

3 nuclear (cell soma), 2 plexiform (synaptic connections), 1 nerve fiber layer

  1. photoreceptor outer segments (OS)
  2. outer nuclear layer (ONL): photoreceptor somas
  3. outer plexiform layer (OPL): photoreceptor / bipolar / horizontal cell synapse
  4. inner nuclear layer (INL): horizontal, bipolar, and amacrine cell somas
  5. inner plexiform layer (IPL): bipolar / amacrine / ganglion cell synapses
  6. ganglion cell layer (GCL): ganglion cell somas
  7. nerve fiber layer (NFL)
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27
Q

what is the pigmented epithelium made of? what do they do?

A

melanin-containing cells behind photoreceptors

  • acts as backstop for light
  • maintains phototransduction machinery of photoreceptors by recycling of PR discs
  • pigment regeneration
  • photoreceptor nnourishment
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28
Q

what are examples of retinal glia cells and where are they?

A

astrocytes - neurovascular
microglia - immune system
Mueller cells - radial glia-like in ionic milieu, guidance during development

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29
Q

how does vertical information flow?

A

photoreceptors –> bipolar cells –> ganglion cells

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30
Q

how does lateral information flow?

A

horizontal cells and amacrine cells

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31
Q

how does vertical neurotransmission occur?

A

cells along vertical path (photoreceptors, bipolar, and ganglion cells) release glutamate

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32
Q

how does horizontal neurotransmission occur?

A

cells mediating lateral information transmission (horizontal and amacrine cells) release mostly GABA and glycineric

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33
Q

how many rods or cones do one bipolar cell contact?

A

1 bipolar cell contacts many rods, but only 1 cone

-but one cone will target 2 types of bipolar cells (one inverse and one regular)

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34
Q

what are the 2 classes of photoreceptor? how do their sensitivity and resolution differ?

A

in duplex retina: rods and cones

  • rods: mostly in periphery, with high sensitivity and low resolution (low spatial recognition); high convergence of rods onto rod bipolar cells
  • cones: mostly in fovea, with low sensitivity (no spatial integration) and high resolution; one cone to 1 cone (midget) bipolar cell
35
Q

what are is the general structure of photoreceptor cells?

A

ciliated cells, with outer segment connected to inner segment via connecting cilium

  • outer segment; houses phototransduction machinery
  • inner segment: housekeeping machinery (nucleus, mitochondria, Golgi, ER, etc.)
  • synaptic terminal: contacts bipolar and horizontal cells
  • neurotransmitter: glutamate
36
Q

how do photoreceptors respond to light?

A

in darkness, rods and cones are depolarized near -40mV, and nt is released continuously

  • when stimulated by light, PR don’t fire APs, but instead respond with graded hyperpolarizations
  • hyperpolarizations spread passively to synapse where it reduces release of glutamate
37
Q

what is the PR circulating current in the dark?

A
  • Na+ and Ca++ flow inward through cGMP-gated channels at outer segment, depolarizing cell
  • K+ flow outward through K+selective channels at inner segment, hyperpolarizing cell
  • combined effects cause steady, depolarized membrane potential of -40 mV
38
Q

what is the PR circulating current in the light?

A
  • absorption of light reduces cGMP levels in outer segment
  • cGMP is intracellular transmitter of phototransduction
  • cGMP-gated channels close, reducing inflow of Na+ and Ca++
  • K+ continue to flow out of inner segment, continuing hyperpolarization, reducing glutamate released
39
Q

what are light-induced reductions in Ca++ levels important for?

A

light adaptation

40
Q

when does phototranduction begin? what happens?

A

when a pigment molecule absorbs a proton

  • active rhodopsin (R*) initiates a series of biochemical reactions (phototransduction cascade) leading to reduction in cGMP levels
  • provides high amplification which allows rods to respond to absorption of a single H+
41
Q

how many cGMP channels does 1 R* close?

A

1 active rhodopsin closes ~200 cGMP channels

42
Q

what is phototransduction?

A

process by which light is converted into electrical signals

43
Q

how are pigments activated in phototransduction?

A
  • disk membranes packed w/ primary light detector (visual pigment PRO rhodopsin, cone opsin)
  • rhodopsin made of opsin molecule w/ light-absorbing chromophore 11-cis retinal (vit A aldehyde)
  • absorption of a photon changes conformation of retinal from 11-cis to all-trans
  • conformational change in retinal leads to activation of rhodopsin (R to R*)
  • when activated, catalyzes activation of heterotrimeric G-PRO transducin
  • R* initiates biochemical reactions that reduce cGMP levels
  • retinal binds covalently inside pocket formed by opsin molecule
  • all-trans retinal breaks covalent bond and exits pocket in opsin molecule
44
Q

what are opsins members of? what is rhodopsin?

A

GPCR superfamily of signal transducing receptors

  • rhodopsin is the cone opsin
  • opsin tunes absorption of light to particular region of spectrum
45
Q

how is phototransduction amplified?

A

absorption of single H+ closes more than 200 channels

  • leads to membrane hyperpolarization of 1 mV
  • careful observers can see light flashes so dim that only 1 in 100 rods absorb single photon
46
Q

what is dark adaptation?

A

restoration of sensitivity after exposure to illumination

  • restoration of retinal (convert from all-trans to 11-cis isomere)
  • occurs in retinal pigment epithelium in visual cycle
47
Q

what is the visual (retinoid) cycle? where does it occur?

A

essential for maintaining light sensitivity in photoreceptors by restoring retinal to form capable of signaling photon capture
-occurs largely in pigment epithelium

48
Q

what are the steps of the visual cycle?

A
  1. after absorbing photon, all trans-retinal dissociates from opsin and is transported to pigment epithelium
  2. re-isomerizes itself back to 11-cis retinal
  3. chromophore 11 cis-retinal is transported back to outer segment where it recombines with opsin to form pigment
49
Q

what does the fovea do for higher acuity?

A

pushes away ganglion cells, IPL, and INL (inner plexiform and nuclear layers)

50
Q

how does the population of fovea VS periphery differ in terms of photoreceptors?

A

fovea is highly populated by cones, while periphery has mostly rods
-in periphery, the cones are larger and more spread apart

51
Q

how do the functional specializations of rods and cones differ?

A

rods: very sensitive to light, respond to absorption of single photon, pool signals from 15-30 rods, tradeoff high sensitivity for low spatial resolution, most numerous
cones: less sensitive (tradeoff high spatial resolution for low sensitivity), need ~100 photons to elicit response, mediate high-acuity vision, color vision

52
Q

what is scotopic vision?

A

rod only vision

-high sensitivity, low acuity, no color

53
Q

what is photopic vision?

A

cone only vision

-low sensitivity, high acuity, color

54
Q

what is mesopic vision?

A

cone and rod vision active together

55
Q

retinitis pigmentosa

  • what it is
  • risk factors
  • symptoms
  • treatment
A

a group of genetic eye conditions that lead to incurable blindness (1:4000)

  • mutation of 100+ genes for rhodopsin and other rod PRO, leading to degeneration of rods and (unknown) cones –> pigment spicules and atrophied vascularization
  • night blindness, then tunnel vision, often legally blind by 40 yo, plus loss of ERG response
  • no treatment and no known risk factors
56
Q

what is the ERG?

A

electroretinogram

  • provides measure of retinal function
  • brief change in potential evoked by large-field flash of light to eye
  • recorded w/ contact lens electrode
  • reflects “mass” activity of retinal neurons to diagnose retinal pathologies
  • in normal eye, will have specific wave form, but retinitis pigmentosa will have no response
57
Q

age-related macular degeneration

  • what it is
  • risk factors
  • symptoms
  • treatment
A

leading cause of vision loss (10% >50, 33% >75)

  • wet and dry AMD
  • RF: aging, smoking, genetics, local inflammation from complement system
  • symptoms: loss of central vision and acuity
  • treatment: differs for wet/dry
58
Q

what is wet AMD and what is the treatment?

A

abnormal blood vessels behind retina grow under macula, leaking and rapidly damaging retina (choroidal neovascularization)
-treat with laser coagulation of vessels and intravitreal infection of anti-neovascular agents

59
Q

what is dry AMD and what is the treatment?

A

RPE and photoreceptors of macula degenerate, accumulation of drusen (yellow deposits of cellular debris) that atrophies central retina; 85% of AMD
-treat w/ antioxidants to slow progression

60
Q

diabetic retinopathy

  • what it is
  • risk factors
  • symptoms
  • treatment
A

retinal damage from DM; can be proliferative or non-proliferative

  • RF: in 80% of patients w/ DM for 10+ years
  • symptoms: no warning sides if early, but cause blurry vision w/ macular edema; new vessels bleed into retina and block vision
  • treatment: laser surgery to reduce edema and injecctions w/ anti-neovascular factors
61
Q

how do proliferative and non-proliferative diabetic retinopathy differ?

A

proliferative: new, fragile vessels grow, which leak blood
non-proliferative: hyperglycemia-induced pericyte death leads to incompetence of vascular walls, microaneurysms, and “dot-and-blot” hemorrhages, with vascular beading and ischemia (cotton wool spots)

62
Q

what is spatial contrast in regards to the visual system?

A

detects light/dark differences

-can be spatial/luminance, color, spatial/color, motion, depth, optic flow, curvature, etc.

63
Q

what is the receptive field?

A

area of the retina (sensory stimulus space) that, when stimulated, elicits change in response of neuron (stimulus response)

  • for a visual neuron, it means that the position in visual space where a change of light causes change in activity of that neuron
  • divided into “on center” and “off center” neurons
64
Q

how do on and off center cells differ?

A

on center: increase discharge rate to luminance increments in receptive field center (so APs increase when light is shone in the center, and decrease with darkness and light in antagonistic surrounding)

off center: increase discharge to luminance decrements in receptive field center (so APs increase when center light is turned off, there’s dark in the center, or light is in the antagonistic surrounding)

65
Q

what is a fundamental receptive field property of retinal ganglion and bipolar cells?

A

center/surround organization

  • center-surround antagonistic receptive fields emphasize regions where there are differences in illumination (edges)
  • so GCs whose firing rate is most affected by edge are those whose receptive fields lie along border of illumination
66
Q

where do the functional differences between on and off center GCs arise?

A

at the synapse between photoreceptors and bipolar cells in OPL (outer plexiform layer), the first synapse in the visual system

67
Q

when do ON and OFF BCs depolarize and hyperpolarize? how is this determined?

A

ON BC depolarize to light, hyperpolarize to dark
OFF BC hyperpolarize to light, depolarize to dark

glutamate receptors on bipolar cells determine center properties and of those of ganglion cells they innervate
-graded depolarization of BCs leads to increased glutamate release at synapses and depolarization of GC they contact

68
Q

how are center-surround receptive fields constructed?

A

antagonistic surround of GC receptive fields is product of lateral interactions in OPL by horizontal cells and IPL by amacrine cells

  • HC inputs establish surround component of RF of bipolar cell (and ganglion cell it’s attached to)
  • cones synapse on bipolar cells to form RF centers and H-cells to form RF surrounds
  • antagonistic surround inhibits center response (spreads laterally)
  • input from HCs oppose changes in membrane potential of photoreceptors induced by phototransduction
69
Q

what does color add?

A

perceptual dimension to differentiate objects when differences in luminance are subtle or non-existent
-color facilitates detecting borders or objects

70
Q

what is the difference between dicrhomatic and trichromatic?

A

di: most mammals, differentiate green/blue
tri: humans, differentiate red/green/blue

71
Q

what are the three cone types and their colors in trichromacy?

A

L(ong) = red, M(edium) = green, S(hort) = blue

  • refer to wavelengths
  • opsin sequence tunes absorption of light to a particular region of spectrum
  • L is quite different from M and S, but M and S are similar
72
Q

cone mosaic

A

far from uniform, regular, or evenly populated between individuals

  • only 5-10% of cones are S-cones
  • large differences in ratio of M and L don’t have severe impact on color perception
73
Q

partial color blindness facts

  • what it is
  • symptoms
  • treatment
A

6-8% of males, 0.4% of females exhibit some color deficiency

  • abnormal red/green vision due to genes coding for red/green cone opsins
  • no treatment, b/c not progressive retinal disease
74
Q

what is deuteranopia?

A

no expression of M opsin (green pigment)

75
Q

what is protanopia?

A

no expression of L opsin (red pigment)

76
Q

what is tritianopia?

A

no expression of S opsin (blue pigment)

-not X-linked and relatively uncommon

77
Q

what pathways do the ganglion cells form?

A

3 distinct anatomical parallel pathways to brain, plus 2 (on/off) physiological paths
-parvocellular, magnocellular, and koniocellular pathways

78
Q

parvocellular pathway origin

A

originates in P (color opponent) ganglion cell

79
Q

magnocellular pathway origin

A

originates in M (luminance encoding) ganglion cell

80
Q

koniocellular pathway origin

A

small bistratified yellow-blue ganglion cells (blue on, yellow off)

81
Q

what are M cells?

A

in periphery w/ large receptive fields

  • good light and contrast sensitivvity and temporal resolution (sensitive to motion)
  • not color sensitive
  • large cells receive input from large number of photoreceptors
  • origin of magnocellular pathway
82
Q

what are P cells?

A

midget cells; small receptive fields

  • provide high acuity and color sensitivity
  • poor light and contrast sensitivity
  • opponent color receptive fields
  • in fovea, a P ganglion cell receives input from a single bipolar cell that receives input from a single cone
  • origin of parvocellular pathway
83
Q

what are K cells?

A

bi-stratified ganglion cells

-carry S info (blue)

84
Q

color opponent receptive fields?

A

outputs of 3 cone types are encoded in retinal circuitry into 2 color opponent pathways: red VS green and blue VS yellow (green + red)
-color/wavelength info can only be determined through comparisons between 2+ cone types, thus opponency