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Phototransduction And Visual System Physiology Flashcards

1
Q

What are the photoreceptors?

A

Rods and cones

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2
Q

What is rod mediated vision also called?

A

Scotopic vision

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3
Q

What happens when you lose rod vision ?

A

Night blindness

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4
Q

What stimulates rod cells?

A

SINGLE photon

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5
Q

What do rods converge onto?

What does this allow?

A

MANY rods to a SINGLE bipolar cell

Allows for high level of sensitivity (but low resolution)

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6
Q

After the rod cells converge onto the bipolar cell, what will that synapse on?

A

Single amacrine cell

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7
Q

What is cone mediated vision also called?

A

Photopic vision

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8
Q

What happens when you lose cone vision ?

A

Legally blind

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9
Q

What activates cones?

A

~100 photons

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10
Q

What do cones converge onto?

What does this allow for?

A

One cone cell —> one bipolar cell

Best resolution (low sensitivity)

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11
Q

What is mesopic vision?

A

When both rods and cones are activated by the light levels of environment

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12
Q

What is the dark current?

A

When it is dark,

The cells are constantly depolarized and release glutamate

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13
Q

What will suppresses the dark current?

What will this cause?

A

Light

Causes hyperpolarization of cells
Reduced release of Glu

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14
Q

When is the release of glutamate the hgihest?

Why? M

A

When it is dark

Because this will activate the off center bipolar cells (those for dark vision)

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15
Q

When is release of glutamate lowest?

Why?

A

When there is light

Low glutamate activates On center bipolar cells

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16
Q

What are amacrine cells needed for?

A

Low light pathways

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17
Q

When does night blindness occur?

A

When th rod mediated release of glutamate is disrupted

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18
Q

What kind of potentials do neuronal cells of the retina use?

Why?

A

Graded potentials

So there can be varying streams of glutamate

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19
Q

What kind of potentials do ganglion cells use?

A

Action potentials

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20
Q

What are the two subtypes of bipolar cells?

A

On center & Off center

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21
Q

What glutamate receptor do ON-center bipolar cells have?

What kind of receptor is this? Connected to what?

A

MGLuR6

metabotropic - connected to Gi

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22
Q

Due to the mGLuR6 receptors on ON center bipolar cells, what will occur when glutamate is decreased?

A

Gi is no longer active

Open cyclic CMP gated Na/Ca Channels and increases cations

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23
Q

What will lots of glutamate do ON center bipolar cells?

A

Will allow Gi to be active

Gi will close cyclic CMP gated na channel and decrease cations

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24
Q

What are the receptors on OFF center bipolar cells?

What type of receptor are these?

A

Normal glutamate receptors (non-NMDA Rs = AMPA R.)

Ionotropic

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25
Q

What happens when it is dark out?

A

Glutamate is increased

Binds to AMPA r. On OFF center bipolar cell
(Active w/ glu binidng)
—> depolarization —> off center ganglion cell —> optic nerve

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26
Q

What are the varieties of ganglion cells?

A

On and off center ganglion cell

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27
Q

What are the Rs. Of ganglion cells?

A

NMDA or non-NMDA rs.

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28
Q

What makes up hte fibers of the optic nerve?

A

Ganglion cell axons

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29
Q

Where will ganglion cells go to?

A

To the cortex where they will release glutamate

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30
Q

What do amacrine and other horizontal cells secrete?

Excitatory or inhibitory?

A

Release glycine or GABA

Inhibitory

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31
Q

What is the role of amacrine cells?

A

Allows us to see in low light conditions to enhance edges, shadows, and contrasting areas of luminance

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32
Q

What is the direct target of the retina?

A

Lateral geniculate body

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33
Q

How is the Lateral geniculate body organized?

A

Retinotopically

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34
Q

How are the signals from each eye composed at the lateral geniculate body?

A

Signals are kept separate here

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35
Q

What are the functions of the Lateral geniculate body?

A

Control motion of eyes to converge on a point of interest

Control focus of eyes based on distance

Determine relative position of objects to map them in space

Detect movement relative to an object

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36
Q

What does the superior colliculus create?

A

Map of visual space to activate appropriate motor responses required to move eyes

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37
Q

What is the funciton of the supeiror colliculus?

A

Coordinate head and eye movements to visual targets

Reflexive saccades

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38
Q

What does the Pretectum do?

A

Reflex control of pupil and lens

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39
Q

Where does the Pretectum send projections to?

A

Edinger westphal nucleus (for pupil)

and then to ciliary ganglion (for lens)

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40
Q

What forms the retinohypothalamic tract?

Where does this tract go?

What does it control?

A

Fibers branching off optic tract

To supraoptic, suprachiasmatic and paraventricular nuclei of hypothalamus

Gives visual input to hypothalamus to allow regulation of circadian rhythms etc.

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41
Q

What are the neurons of the medial temporal area/V5 responsive to?

Allowing us to what?

A

Direction of moving edge

Track motion across a scene

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42
Q

Does the MT/V5 area recognize color?

A

No - ignores it

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43
Q

What is cerebral akinetopsia?

What causes it?

A

Motion blindness - knows things are moving (V3), but movements are broken up

Lesion to MT/V5

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44
Q

What is the accessory optic system?

A

Several small nuclei involved in advanced visual process

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45
Q

What is the role of the accessory optic system?

A

Impt. Role in eye movements of Compensation and Pursuit (particularly w/ alternating saccadic type eye movements)

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46
Q

What is the major job of V1?

What else is this known as?

A

Identifying edges and contours of objects; constructs image features like size, orientation, local direction of movement and binocular disparity

Primary visual cortex or striate cortex

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47
Q

Where is V1?

What does it consist of?

A

Occipital lobe

6 cortical layers

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48
Q

How is V1 organized?

A

Retinotopically

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49
Q

Is V1 excitatory or inhibitory? W/ what NTRs?

A

Mostly excitatory w/ glutamate

Also has some GABA interneurons

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50
Q

What is V2 for?

A

Depth perception by analyzing disparities b/w eyes

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51
Q

What is V3a for?

A

Ids that motion is indeed occurring

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52
Q

What is V4 for?

A

COMPLETE processing of color

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53
Q

What are ocular dominance columns?

A

Columns running thru all 6 layers of cortex

W/ each one having a preference to input from one eye or another

54
Q

How are ocular dominance columns mapped?

A

Into stripes

55
Q

What are orientation columns?

A

Organizers region of neurons that are excited by VISUAL LINE STIMULI of VARYING ANGLES!

56
Q

How are orientation columns oriented?

A

Perpendicular to the cortical surface

57
Q

What are vertically responsive orientation column responsive to?

A

Vertical images (i.e. a tall tree)

58
Q

How are orientation columns mapped?

A

Into swirls

59
Q

What are the Blobs in V1?

A

Regions of neurons that are sensitive to COLOR assemble into cylindrical shapes

60
Q

What is the difference in V1 and V4 processing of color?

A

V1 = subconscious awareness of color but cannot identify it

V4 = conscious awareness of color

61
Q

What do you need for accurate color detection?

A

All 3 kinds of cones

62
Q

What is cerebral achromatopsia?

A

Color loss bc damage to specific extrastriate cortical areas (V4)

Patient cannot see info supplied by retina (color blindness at level of retina)

63
Q

What is color blindness?

A

No color Bc CONES do not funciton properly

64
Q

What are melanopsin ganglion cells?

A

Specialized photosensitive ganglion cells that contain melanopsin

65
Q

What are considered a 3rd class of photoreceptors in retina?

A

Melanopsin ganglion cells

66
Q

Where do melanopsin ganglion cells project to?

A

Suprachiasmatic nucleus of hypothalamus
Light sensitive nucleus of pretectum
Limbic system

67
Q

What do melanopsin ganglion cells not project to?

Making them be called what?

A

Do not project to visual cortex

—> non-image forming light responsive melanopsin gnaglion cells

68
Q

What do melanopsin gnaglion cells do?

A

Helps regulate circadian rhythms, mood, and sleep

69
Q

What therapy is good for those who experience shifts in light/dark cycles?

Because of what system

A

Light therapy

Bc of melanopsin ganglion cells

70
Q

What is the ventral pathway that arises form the visual cortex?

A

From V1 —> V4 —> temporal lobe

71
Q

What is the function of the ventral pathways?

A

Involved in interpreting images (recognizing or copying shapes, forms, faces)

Copying/naming objects = separate function in temporal lobe

Facial recognition = special area

72
Q

What is the ventral pathway selectively activated by?

A

Shape, color, texture and object recognition

73
Q

What is the dorsal pathway from the visual cortex?

A

From V1 —> V2 —> V3 —> V5/MT —> Parietal lobe

74
Q

What is the function of the dorsal pathway?

A

Pathway allows you to complete motor actions based on visual input thru this pathway

75
Q

What is the dorsal pathway selectively activated by?

A

Directionality and speed

76
Q

What is the ventral pathway called?

The dorsal pathway?

A

Ventral = vhat

Dorsal - where

77
Q

What does damage to the inferior temporal lobe cause?

Due to what?

A

Agnosia and prosopagnosia

Due to interruption of the ventral stream

78
Q

What is agnosia?

A

Can see object but unable to copy or name it

Cannot see parts of objects contributing to it as a whole

Cannot interpret, understand or assign meaning

79
Q

How is agnosia clinically seen?

A

Inability to construct or draw visual stimuli

Cannot recognize a picture of object

80
Q

What is prosopagnosia?

A

Agnosia where you can identify a face as a face but NOT FACE AS BELONGING TO A PERSON

81
Q

What do rod cells contain?

A

Contain rhodopsin

82
Q

Where are rod cells concentrated?

A

Just outside the center of the fovea

83
Q

How are rod cells positioned around cone cels?

A

Hexagonally packed around cones

84
Q

How is the outer segment of rods constructed?

A

Disc membranes stacked in outer membrane w/ structure protein peripherin

85
Q

What system are rod cells associated with?

Pathway?

A

W/ GPCR system

Rhodopsin —> transducen —> cGMP PDE

86
Q

What is on the surface membrane of Rod cells?

A

Na/Ca exchanger
GC
cGMP gated Na channel

87
Q

What are the desensitization proteins associated with rod cells?

A

Beta arrestin

Rhodopsin kinase

88
Q

In the dark, hwo are rod cell membranes?

A

Partially depolarizes bc glutamate is continuously released (inhibiting optic nerve ON center bipolar cells)

CGMP na channel is open and cell is depolarized

89
Q

How are rod cells’ channels in hte light?

A

Sodium channels = closed

Cell = hyperpolarized

Bc cGMP is hydrolyzed

90
Q

What happens when the rod cell is hyperpolarized in the LIGHT?

A

Stops glutamate transmission

Depolarizes On center
Hyperpolarizes Off center cells

91
Q

What is rhodopsin homologous to?

A

Beta adrenergic receptors

92
Q

What is covalently bound to 11-retinal on rhodopsin?

A

Lysine 296 in center of 7 TM

93
Q

What is retinal derived from?

A

Vitamin A

94
Q

What is the active rhodopsin player have?

What can it absorb?

A

Protonated schiff base

> 440 nm

95
Q

What makes up rhodopsin?

A

Opsin + retinal

96
Q

What is the activation form of retinal?

A

11 trans retinal

97
Q

Where are cones concentrated?

A

Fovea

98
Q

What are the three varieties of cone receptors? At what wavelength do they absorb?

A 
Blue =    460 nm
Green =   520 nm 
Red =   > 560 nm
99
Q

What chromosomes are the photoreceptor proteins from?

A

Rod - chromosome 3

Blue - chromosome 7

Red - chromosome x

Green - chromosome x

100
Q

What is the heritability pattern for red green color blindness?

A

X linked recessive trait

101
Q

What modulated cGMP PDE?

A

Transducen

102
Q

What will light activate?

A

Transducen (Gt), causing alpha subunit to dissociate —> activate cGMP PDE

103
Q

What will cGMP PDE do?

A

Catalyze hydrolysis of cGMP to 5’GMP

104
Q

What will low cGMP cause?

A

Activation of GC

Hyperpolarization of visual cells

= no visual signal tranduciton

105
Q

What is the role of calcium in the visual phototransduction pathway?

A

Controls rate of cGMP synthesis and governs rate by which system is restored

106
Q

When Ca is low, is GC active or inhibited?

A

Active

107
Q

When it is dark, what is calcium doing?

A

Ca and Na enter Rod thru cGMP gated Na channels

108
Q

What balances the calcium influx?

A

Calcium channel exchanger

One ca out, for 4 na in/1 k out

109
Q

When it is dark, what is calcium doing?

A

Ca does not come in thru cGMP gated Na Chanel’s

But exchanger channel still working = Calcium level drops

110
Q

What will the drop in calcium stimulate?

A

GC

111
Q

What will GC do?

A

Increase the concentration of cGMP and open cGMP gated Na channels

112
Q

What is the pathway of the visual phototransduction system when there is light?

A 
One photon to rhodopsin 
Trasnducin activated, alpha subunit dissociates
Activates cGMP PDE 
Hydrolyzes cGMP to GMP 
Decreases {cGMP}
CGMP gated Na channels closed 
Drop in calcium 
Membrane potential altered by 1 mv 
Signal relayed to brain

(Drop in calcium stimulates GC, which restores {cGMP} and re-opens cGMP gated Na/Ca channel)

113
Q

What are the 3 ways to terminate signals of the visual phototransduction pathway?

A
  1. Light activated rhodopsin blocked from activating transducen by Arrestin
  2. ATP is hydrolyzes to ADP, therefore alpha subunit cannot be bound to PDE
  3. Increased cGMP by GC
114
Q

How is arrestin allows to bind rhodopsin?

A

Bc rhodopsin kinase phosphorylates C terminus of Meta-rhodopsin at Thr and Ser

115
Q

What are the dietary sources of vitamin a?

A 
Carrots
Leafy greens
Sweet potatoes 
Squash
Broccoli
Animal products (eggs, dairy, fish, liver)
116
Q

What could deficiency of vitamin A cause?

A 
‣ Night blindness
‣ Xerophthalmia		
‣ Ckeratinization of epithelium 
‣ Dry, scaly skin
‣ Failure of wounds to heal well 
‣ Adv. Macular Degeneration
‣ Leading cause of preventable blindness in children
‣ Bitot’s spots
117
Q

What are bitot spots?

A

Build up of keratin debris superficially in conjunctiva

Usually foamy in appearance

118
Q

What can an excess of vitamin a cause?

A

Liver toxicity and joint pina

119
Q

What can infantile exposure to isotretinoin in womb?

A

Cleft palates

Heart abnormalities

120
Q

What nutritional disorder affects the cornea the most ?

A

Vitamin A deficiency

121
Q

If you are deficient in vitamin A, how will the cornea present?

A

Bitot spots

Xerosis

Keratomalacia

122
Q

What is xerophthalmia?

A

◦ Abnormal dryness of conjunctiva and cornea of eye

‣ W/ inflammation and ridge formation

123
Q

What is nyctalopia?

Caused by ?

A

Night blindness; difficulty seeing in lowlight

Disorder of rod cells - assoc. w/ a vitamin a deficiency leading to insufficient rhodopsin

124
Q

What is corneal or conjunctival xerosis?

A

◦ Metaplasia of conjunctival epithelium to stratified squamous type; keratinized surface

125
Q

What are bitot spots ?

A

◦ Tangles of keratin mixed w/ saprophytic bacteria and sometimes fungi

126
Q

What is macular degeneration?

A

Degeneration of RPE and retina

127
Q

How does macular degeneration present?

A

Loss of central field vision

Poor night vision

Atrophy, macular hemorrhage, pigmentation, macular edema, and subretinal fluid

128
Q

What is the role of macular carotenoids?

What are the macular carotenoids?

A

play a direct role in protection of retina against damage

  • Lutein
  • Zexanthin
129
Q

Why is the eye susceptible to macular generation?

A

‣ Has high O2 flux and resp. Quotient
‣ High lipid content
‣ High glucose content
‣ UV radiation

130
Q

What are the two types of AMD?

A

Dry type atrophy of macula

wet AMD assoc. w/ VEGF

131
Q

What is the etiology of macular degeneration?

A

‣ Combo of envir. And genetics change REP oxidatively and thru inflammation
• Induces angiogenesis and increases inflammation and vascular permeability

‣ Genetics:
• 19 genes ID’d
• Dysregulation of alternate complement system
• Mutation in ABCA4 can cause macular degeneration

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