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Neuro I > Lecture 10: Biochemistry of Vision > Flashcards

Lecture 10: Biochemistry of Vision Flashcards

1
Q

What are the 3 main cell types of the eye?

A
  1. Photoreceptors
  2. Interneurons (bipolar cells, horizontal cells, amacrine cells)
  3. Ganglion cells
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2
Q

What are the 3 main components of the retinal circuit for the processing of visual signals?

A

Photoreceptors —> Interneurons —-> Ganglion cells

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3
Q

What are the output cells of the retina and what do their axons form?

A
  • Ganglion cells
  • Axons form the optic nerve
  • Project to the brain
  • Information transmitted via AP’s
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4
Q

How do the photoreceptors differ in rods vs. cones; what is the sensitivity and resolution like in each?

A

Rods (night vision)

  • Rhodopsin (cannot detect color)
  • High sensitivity and low spatial resolution

Cones (color detection)

  • Three opsins (red, green, and blue)
  • Low sensitivity and high spatial resolution
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5
Q

What are the 2 components of Rhodopsin?

A

Opsin (protein) + 11 cis-retinal (derived from Vitamin A)

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6
Q

The structure of Rhodopsin is very similar to what receptor?

A

β2-adrenergic receptor

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7
Q

How is retinal able to form the protonated schiff base of functional rhodopsin?

A
  • Lysine-296 in opsin (located in the 7th TM of the protein) covalently bound to 11-cis retinal

- Aldehyde of retinal forms Schiff base with amine of lysine

  • Schiff base becomes protonated
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8
Q

What is the absorption wavelengths of free retinal vs. un-protonated schiff base retinal, and protonated schiff base retinal?

A

Free retinal: 370 nm

Un-protonated: 380 nm

Protonated: 440 nm +

*Rhodopsin absrobs maximally at 500 nm

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9
Q

What occurs once a photon hits rhodopsin?

A
  • 11-cis-retinal —> 11-trans-retinal (isomerization)
  • Causes 5Å conformational change of Schiff-base Nitrogen
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10
Q

What is the activated form of Rhodopsin called?

A

Metarhodopsin II

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11
Q

Explain the visual signal transduction pathway after the photon is absorbed by Rhodopsin in a photoreceptor cell?

A
  • Light absorbed by rhodopsin in photoreceptor cell, which interacts with the retinal causing 11-cis —> 11-trans
  • Conformational change of rhodopsin —> Metarhodopsin or R*
  • R* interacts w/ G protein transducin, catalyzing its activation by the release of bound GDP in exchange for GTP
  • The alpha subunit of transducin disassociates from its β and γ subunits and activates phosphodiesterase, which hydrolyzes cGMP
  • Lowered cGMP levels close the cGMP-gated Na+ channels leading to hyperpolarization of the cell and neuronal signaling
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12
Q

How does each step of the visual signal transduction contribute to the sensitivity of our eyes to light?

A
  • At each step of the process, there is significant amplification
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13
Q

What are the signal termination steps which block light-activated rhodopsin from activating transducin?

A
  • Rhodopsin kinase phosphorylates COOH terminus of Metarhodopsin II at Thr and Ser allowing binding by Arrestin and preventing the interaction with Transducin
  • Transducin has intrinsic GTPase activity and hydrolyzes GTP to GDP causing dissociation of transducin from PDE and reassociation with the βγ subunits
  • Guanylate cyclase synthesizes cGMP from GTP
  • Elevated cGMP levels re-open cGMP-gated ion channels
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14
Q

Ca2+ inhibits the activity of what enzyme in the signal transduction pathway?

A

Guanylate cyclase

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15
Q

What is the movement of Ca2+ in the rod during dark conditions?

A
  • Ca2+ and Na+ enter the rod OS through cGMP-gated ion channels
  • Ca2+ influx is balances by its efflux through a Na+/K+/Ca2+ exchanger
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16
Q

What is the movement of Ca2+ in the rod during light conditions?

A
  • Ca2+ influx through the cGMP channel stops but exchanger transport continues
  • Reduces intracellular Ca2+ from 500 nM to 50 nM
  • This STIMULATES the activity of guanylate cyclase, restoring [cGMP] and re-opening cGMP-gated ion channels
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17
Q

Rods and cones release what inhibitory NT in the dark when depolarized; why?

A
  • Glutamate
  • Inhibits the optic nerve bipolar cells
  • Quiets the information to the brain
18
Q

When you open your eyes, what occurs to the cell and what effect does this have?

A
  • Causes hyperpolarization
  • The inhibitory NT, glutamate is removed
19
Q

Cone cells are homologues of ______, members of ________ family, use ______ as chromophore.

A

Cone cells are homologues of rhodopsin, members of 7TM family, use 11-cis-retinal as chromophore

20
Q

What are the 3 varieties of cone receptors and what wavelength does each correspond to?

A

1) Blue (460 nm)
2) Green (530 nm)
3) Red (560 nm)

21
Q

When someone is color-blind they cannot distinguish between what 2 colors; what chromosome are the genes for these 2 colors found on?

A
  • Red and green
  • X chromosome
22
Q

Rearrangement of the genes for color during DNA replication may lead to what?

A

1) Loss of visual pigment genes
2) Formation of hybrid pigment genes that encode photoreceptors with anomalous absorption spectra

23
Q

The AA’s most important for determining absorption spectra are in what half of each photoreceptor protein?

A
  • The carboxyl-terminal half of each photoreceptor protein
  • The part of the gene that encodes this region most strongly affects the absorption charateristics of hybrid receptors
24
Q

The purpose of the retinoid cycle is the regeneration of what?

A

11-cis-retinal

25
Q

Explain the basics of the Retinoid cycle from rod cell –> RPE –> rod cell

A

In the rod cell:

  • Light-induced change from 11-cis to all-trans-retinal
  • Release of all-trans-retinal from opsin
  • Enzymatic reduction of all-trans-retinal to all-trans-retinol
  • Export of all-trans-retinol (with help from iRBP)

In the retinal pigmented epithelium (RPE):

  • Uptake into the RPE and translocation to ER for enzymatic processing to 11-cis-retinal
  • Export of 11-cis-retinal

In the rod cell:

  • Uptake of 11-cis retinal into rod cell
  • Covalent attachment (Schiff base) to opsin forming a functional rhodopsin
26
Q

Why are photoreceptors of the outer segment (POS) particularly vulnerable to damage and why is this significant?

A
  • Contains highly reactive retinoids and high levels of unsaturated PLs
  • Rod and cones terminally differentiated post-mitotic cells (DO NOT DIVIDE)
27
Q

How have photoreceptors of the outer segment developed a unique mechanism for renewal?

A
  • Shedding tips which get phagocytosed by RPE
  • In mammals, 10% rods shed/day and same amount of membrane and protein components made ever day
  • Disruption in renewal leads to degeneration
28
Q

OS disk recycling occurs in what type of manner; when is peak rod versus peak cone shedding?

A
  • Occurs in a circadian manner
  • Peak rod shedding in morning
  • Peak cone shedding after dark
29
Q

What occurs when a photoreceptor gets shed, how does the RPE deal with it?

A
  • The retinal pigmented epithelium (RPE) ingests the POS, which is surrounded by membrane to make a phagosome
  • Series of fusion events with endosome and lysosome for degradation
  • Some components recycled and reused
30
Q

What is Retinitis Pigmentosa; caused by; affects; and characterized by; ultimately what does this lead to?

A
  • Group of inherited retinopathies
  • Caused by mutations in rhodopsin and other photoreceptors protein (peripherin, PDE)
  • Affect disk morphology, photoreceptor structure and function, and renewal
  • Characterized by loss of night vision followed by peripheral vision
  • Leads to degeneration, disease called retinitis pigmentosa
31
Q

Retinitis pigmentosa is characterized by?

A

Loss of night vision, followed by complete blindness

32
Q

What are some of the consequences of Vitamin A deficiency?

A
  • Night blindness
  • Xerophtalmia (dry eye syndrome)
  • Bitot’s spots (due to keratin debris in conjunctiva)
  • Visual impairment
33
Q

What is the mainstay of therapy for Vitamin A deficiency; is too much Vitamin A a bad thing?

A
  • Mainstay of therapy for a deficiency is Vitamin A supplementation
  • Excess Vitamin A due to copious intake of supplements causes liver toxicity and joint pain
34
Q

Night blindness can be caused by?

A
  • Deficiency of Vitamin A
  • Glaucoma

- Cataracts

- Retinitis pigmentosa

35
Q

Age-related macular degeneration (AMD) effects which part of the retina?

A

Effecys the macular region of the retina

36
Q

What plays a key role in the development of age-related macular degeneration (AMD)?

A

Pathological processes in lipid metabolism, oxidative stress and inflammation

37
Q

Age-related macular degeneration (AMD) is clinically divided into what 2 forms and what are the characteristics of each; which of the 2 is most common?

A

1) Dry Form: characterized by accumulation of lipid rich extracellular deposits, degenration of RPE, and secondary photoreceptor loss

2) Wet Form:associated withchoroidal neovascularization. Less common, results in severe vision loss

38
Q

Mutations in what enzyme is related to many vision diseases and what are they?

A
  • Mutation in ATP binding cassette transporter or ABC transporter
  • Stargardt’s disease (autosomal recessive forms of juvenile degeneration)
  • Cone-rod dystrophy
  • Retinitis pigmentosa
  • AMD
39
Q

Explain what effect mutations in ABC transporters play in the development of vision diseases?

A
  • Elevated levels of diretinoid-pyridinium-ethanolamine (A2E), the ultimate product of condensation of 2 molecules of all-tran-retinal and one molecule of phosphatidylethanolamine
  • Also accumulation of all-trans-retinal
  • Accumulation of these 2 produces cellular debris, which in turn generates oxidative stress
40
Q

What are 2 macular carotenoids that have shown to lower the risk of AMD?

A
  • Lutein
  • Zeaxanthin

*Both are free-radical scavenging agents and anti-oxidant compounds

Neuro I (15 decks)

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