- cornea - aqueous humor - lens - vitreous humor

- transduction=transformation of light energy into neuron activity - light causes hyperpolarization of photoreceptors - more intense flash response causes larger hyperpolarization - dark: Na+ influx, K+ efflux, depolarization - light: reduced Na+ influx, K+ efflux, hyperpolarization

- outer segment of photoreceptors are filled with stacks of disc membranes - disc membranes covered with opsins - Rods have rhodopsin - cone have opsins (S, M, L) - vertebrate opsins are closesly relation to metabotropic NT receptors (7TMD)

- rhodopsin has a chromophore called retinal covalently bound to its 7th transmembrane domain - activation: isomerization of retinal causes conformation change in rhodopsin - activated rhodopsin has a conformation that exposes a binding pocked which interacts with the G protein Transducin (Gat)

- GEFs: facilitate release of GDP - increases activity due to more Ga-GTP - ligand bound GPCR acts as a GEF - GDIs: inhibit release of GDP - decrease activity: less Ga-GTP - GAPs: activate intrinsic GTPase activity - decrease activity: less Ga-GTP - GIPs: stop intrinsic GTPase from working - increase activity: more Ga-GTP

- light activated opsin causes Transducin to Exchange GDP for GTP - transducin dissociates - a subunit activated phosphodiesterase - decreased cGMP causes cGMP gated channels to close - causes hyperpolarization because Na+ and Ca2+ cannot enter cell

- phototransduction adjusts its magnitude to prevailing light levels - prevents signal saturation, where all cGMP gated channels are closed

Phototransduction Flashcards by allie parry

Anatomy of the eye - Neural components

retina
- fovea
optic disk
optic nerve

How well did you know this?

Not at all

Perfectly

Optical components

cornea
aqueous humor
lens
vitreous humor

How well did you know this?

Not at all

Perfectly

Supporting components

uveal tract
- choroid
  - pigmented epithelium
- ciliary body
- iris
sclera

How well did you know this?

Not at all

Perfectly

Focusing images on the retina

cornea: provides 80% of the focusing power
- cannot change shape
lens: provides 20% of focussing power
- thin lens: less light bending (far objects)
- thick lens: more light bending (near objects)
shape of the lens is controlled by the ciliary muscles
- relax: thin lens (far sight)
- contracted: fat lens (near sight) accommodation

How well did you know this?

Not at all

Perfectly

Organization of the retina

Distal
-pigment epithelium
-photoreceptor outer segments (rods and cones)
-outer nuclear layer
-outer plexiform layer
-inner nuclear layer
-inner plexiform layer (amacrine, bipolar, horizontal cells)
-ganglion cell layer
-nerve fibre
Proximal

How well did you know this?

Not at all

Perfectly

Phototransduction

transduction=transformation of light energy into neuron activity
light causes hyperpolarization of photoreceptors
more intense flash response causes larger hyperpolarization
dark: Na+ influx, K+ efflux, depolarization
light: reduced Na+ influx, K+ efflux, hyperpolarization

How well did you know this?

Not at all

Perfectly

Light transduction

outer segment of photoreceptors are filled with stacks of disc membranes
disc membranes covered with opsins
- Rods have rhodopsin
- cone have opsins (S, M, L)
  - vertebrate opsins are closesly relation to metabotropic NT receptors (7TMD)

How well did you know this?

Not at all

Perfectly

Rhodopsin

rhodopsin has a chromophore called retinal covalently bound to its 7th transmembrane domain
activation: isomerization of retinal causes conformation change in rhodopsin
- activated rhodopsin has a conformation that exposes a binding pocked which interacts with the G protein Transducin (Gat)

How well did you know this?

Not at all

Perfectly

Transducin activation

transducin is a heterotrimeric G protein
conformational change in rhodopsin triggers a conformational change in Transducins a subunit
- results in:
  1. Decrease in the affinity of the a unit for GDP causing dissociation of GDP from the a subunit, and binding of GTP
  2. Dissociation of BY from a subunit
  3. Release of G proteins from rhodopsin
amplification: more than one transducin can be activated during the time the rhodopsin is bound to all-trans retinal

How well did you know this?

Not at all

Perfectly

G proteins: conformational changes

a subunit:
- nucleotide binding site (also the GTPase region) interacts with 3 switch regions
- when GDP is exchanged for GTP the terminal phosphate group of GTP forms hydrogen bones with side chains of switch 1 and 2 to prevent it from interacting with the loops at the bottom of the GY propeller

-BY subunit doesnt change conformation

How well did you know this?

Not at all

Perfectly

G protein modulation

GEFs: facilitate release of GDP
- increases activity due to more Ga-GTP
- ligand bound GPCR acts as a GEF
GDIs: inhibit release of GDP
- decrease activity: less Ga-GTP
GAPs: activate intrinsic GTPase activity
- decrease activity: less Ga-GTP
GIPs: stop intrinsic GTPase from working
- increase activity: more Ga-GTP

How well did you know this?

Not at all

Perfectly

Process

light activated opsin causes Transducin to Exchange GDP for GTP
transducin dissociates
a subunit activated phosphodiesterase
decreased cGMP causes cGMP gated channels to close
causes hyperpolarization because Na+ and Ca2+ cannot enter cell

How well did you know this?

Not at all

Perfectly

Rods can detect a single photon of light

a single isomerization of retinal starts an enzymatic cascade
1 activated rhodopsin can close 2% of rods cGMP gated channels
changes membrane potential by 1mV

How well did you know this?

Not at all

Perfectly

Photo-cascade inactivation

activated rhodopsin (R*) is phosphorylated on 3 different sites by rhodopsin kinase
- multi site inactivation may yield more uniform Tim course of inactivation (less variability = better signal)
phosphorylated rhodopsin is bound by arresting
arresting binding causes conformation change in R* so that it cannot active Transducin anymore
Transducin is inactivated by RGS9-GB5-R9AP complex
- RGS9 = GAP
- GB5 = Regulatory subunit
- R9AP = membrane anchor

How well did you know this?

Not at all

Perfectly

Light adaption

phototransduction adjusts its magnitude to prevailing light levels
prevents signal saturation, where all cGMP gated channels are closed

How well did you know this?

Not at all

Perfectly

Light adaption mechanism 1

goal: keep some cGMP gated channels open
action: make more cGMP

GUANYLATE CYCLASE
- dark: intracellular Ca2+ inhibits guanylate cyclase activating proteins (GCAPs) (which produces cGMP)
- light: induced closing of cGMP-channels decreases intracellular Ca2+
- drop in Ca2+ up-regulates GCAPs
- GCAPs up regulate guanylate cyclase to produce cGMP
  - fastest and most powerful mechanism
  - also assists in photo cascade inactivation

Light adaption mechanism 2

goal: keep some cGMP gated channels open
action: ensure less PDE activity

RECOVERIN
- Ca2+ biding protein similar to calmoduin
- dark: Ca2+-Recoverin inhibits rhodopsin kinase from phosphorylation great rhodopsin
- light induced drop in Ca2+ relieves this inhibition
- low Ca2+ = more rapid R* inactivation
- less PDE activation
- more cGMP

Light adaption mechanism 3

goal: keep some cGMP gated channels open
action: make channels more sensitive to cGMP

CALMODULIN

dark: Ca2+-Calmodulin binds to cGMP gated channels and desensitizes it to cGMP
light induced drop in Ca2+ = calmodulin dissociates from the channel making it more sensitive to cGMP
- stays open with fewer bound cGMP

Dark adaption

eyes become more sensitive
due to replenishing of 11-cis retinal opsins
retinoids cycle in photoreceptor and pigment epithelium
interphotoreceptor binding proteins (IRBP) chaperones retinoids between photoreceptors and pigment epithelial cells
convert all-trans retinal back to 11-cis retinal in pigment epithelium so they can be reactivated by light

Disc maintenance

photoreceptor disks are continuous being produced
disks migrate from soma toward end of outer segment
old disks removed by pigment epithelium

Specialization of rod and cone systems

rods have high sensitivity, specialized for low intensity vision
cone have low sensitivity, specialized for high sensitive vision
cone transduction specialized for bright light
- reduced amplification in their phototransduction cascade
  - slower/less effective Gat and PDE
- higher expression of RGS9 (GAP)
  - faster inactivation
- cone specific opsin kinase (GRK7)
  - more efficient R* inactivation
- much larger changes in Ca2+
  - engage in Ca2+ feedback mechanisms more rapidly

Specialization of rod and cone systems continued

rods send converging inputs to bipolar cells
- pooling of input leads to greater sensitivity and less acuity
cones have less convergence
- less sensitivity, greater acuity
only cones at fovea
less cones everywhere else
no rods at fovea

Fovea

specialized for high acuity
avascular - no overlaying blood vessels obscuring path of light to the cones
inner retinal cells (bipolar, ganglion, horizontal, amacrine) swept to side so light has unobstructed path to cones
foveal cones thinner than elsewhere
these factors contribute to pit-like structure

Cones and colour vision

human colour vision is trichromatic
short, medium and long cones
short: blue (400 range)
medium: green-yellow (450-550)
long: yellow-red (500-600)

S: only 5-10% of cone population 
   -absent from fovea
   -important for circadian rhythms
M &amp; L: predominant rental cone types
     -proportions vary between humans yet all have normal colour vision

Cones and colour deficiency

- x linked mutations can cause dichromatism - protonopia: missing L cones - deuteranopia: missing M cones - amino acid sequence of each cone opsin determine the wavelength of light its most sensitive to - gradual mutation gave rise to Rhodopsin plus 3 cone types - M and L both on X chromosome and are genetically similar indication recent evolutionary origin - probably from gene duplication - errors in crossing over during meiosis can produce dichromatism