Visual Physiology Flashcards
How is light transmitted through the eye in basic terms?
transmission of light through eye structures (in ocular bulb) to reach the photoreceptors in the retina
excitation of these photoreceptors stimulates (or not) glutamate release which then activates APs in the basal ganglia
these travel along the optic nerve to the primary visual cortex (occipital lobe) to be interpreted as sight
What important structures aid visual capture in the eye?
CHOROID
this provides a highly specialised blood supply to the outer retina
RETINAL PIGMENT EPITHELIUM
located between the choroid and the neural retina, this RPE is also known as the non-neural retina
has multiple functions including light absorption, phagocytic regulation of the outer segments of rods/cones and maintaining the blood-retinal barrier
What are the different layers of the peripheral retina?
outermost (furthest away from vitreous body)
- photoreceptors
- interneurones (bind glutamate and generate APs to transduce signal)
- ganglion cells (strip out the noise and select the salient info for transmission to the brain via APs)
innermost (closest to vitreous body)
What are the 2 main types of photoreceptors?
RODS
night vision
system is more sensitive and phototransduction response is sustained for longer
CONES
day vision
three types: RGB (red, green, blue)
What is the structure of a cone photoreceptor?
2 main sections of cell:
- outer segment (membrane discs containing multilayered phospholipid bilayers like the PM)
- inner segment (cell body and therefore nucleus of cell
Below the cell body of the photoreceptor, there is an “axon” and a synaptic terminal
the “axon” is so-called due to its anatomical structure, but does not fire APs like neurons do
the synaptic terminal is responsible for releasing GLUTAMATE vesicles (upon stimulation)
What is the normal resting membrane potential of a neuron?
-70mV
due to the leakage of K+ ions out of the cells
What is the resting membrane potential of a cone photoreceptor cell?
-45mV
caused by leakage of Na+ into the cell by non-specific cation channels in the outer segment of the cone cells
What is the consequence of having a resting potential of -45mV in cone cells?
much less negative than resting potential for neuron
but not an issue as these cone cells do not fire APs
however, does mean that even at rest, there will be some basal release of glutamate vesicle from the presynaptic termini
What occurs to cone cells when exposed to increased light (brightness)?
cone cell becomes HYPERPOLARISED
(more negative in potential)
this causes closure of the Na+ channels in the outer segments
less glutamate is released from the presynaptic termini
What occurs to cone cells when exposed to reduced light (brightness)?
Cone cell becomes DEPOLARISED
(less negative in potential)
causes opening of Na+ channels in outer segment)
more glutamate is released
What is opsin?
protein component of the colour pigment in the retina
sits on the membrane of membrane disc in the outer segment of cone/rod cells
functions in the initiation of the light response: TRANSDUCTION pathway
in rods, this is rhodopsin
cones: 3 types of opsin proteins (one for each type of colour pigment RGB)
All opsin proteins have a binding site for retinal
What is retinal?
= 11-cis-retinaldehyde (commonly known as retinal)
chromophore derivative of vitamin A
can be in a cis- or trans- conformation
cis-retinal is less stable and therefore more likely to react or be broken down
What is photopigment vs. activated photopigment?
PHOTOPIGMENT
opsin bound to cis-retinal
ACTIVATED PHOTOPIGMENT
opsin bound to trans-retinol
What occurs in the ‘photoisomerisation of retinal’ of light transduction?
Retinal = cis conformation which is less stable that in a trans conformation
(minority of molecules, most are in trans)
when light hits a cis-isomer, the unstable bond is ruptured and the molecule is reformed in its trans conformation
this forms the ACTIVATED PHOTOPIGMENT
What occurs in the ‘amplifying cascade’ of light transduction?
Opsin bound at the membrane disc is a GPCR
binding of retinal at the opsin = activated photopigment
light activation causes conversion to all-trans-retinol (end product) and activation of the attached G-protein
this increases GMP phosphodiesterase activity (leading to increased cGMP hydrolysis/breakdown)
Leads to a fall in [cGMP], which means less are bound to the Na+ channels in open conformation
Na+ channels close, causing change in membrane potential
What is the mechanism regulating the amplifying cascade of light transduction?
= DENSENSITISATION
need the amplification to be transient, so that it can be stimulated from baseline for the next cycle without an after-image
- opsin is inactivated (conformational change due to loss of Ga subunit)
- loss of binding site means that the retinal will fall off
- removal of retinal derivative and destruction
- termination of GPCR cascade
- intracellular [cGMP] rebuilt (by guanylate cyclase)
- allows re-opening of Na+ channels
How does the light transduction cascade differ in rods (vs. cones)?
In rods, the same process happens
just happens more slowly and the GPCR cascade is sustained for longer
more pixels per photon, greater quality ?
How is termination of the transduction cascade terminated?
can be terminated at several levels
e.g. phosphorylation of rhodopsin by rhodopsin kinase
then binding of phosphorylated rhodopsin by arrestin
binding causes quenching of signal (produced by GPCR cascade)
What kind of light changes do photoreceptors respond to?
range of light sensitivity is massive
but will primarily respond to minute changes in brightness from one moment to the next
able to do this by casting aside the absolute quantification of the overall brightness in that situation
due to adaptation process: amends resting potential between light transduction cascades
if the overall light brightness remains the same throughout then the photoreceptor cell will return to it OG baseline (-45mV)
but if the brightness changes, then the basal resting potential will also change to adapt
What mechanisms need to occur in photoreceptors with utmost biochemical precision?
- transduction of the light stimulus
- termination of the light response
- regeneration of photopigment
- controlling the rate and sensitivity of light response (adaptation)
How do photoreceptors control the nature of the light response produced?
Presence of CONTROLLER PROTEINS
these can regulate transducer/enzyme activity
each type of light stimulus will therefore result in a different level of response
e.g. in darker environments, want each photon to produce a bigger response (and vice versa in lighter environments)
What is retinitis pigmentosa?
degenerative disease of the retina, which can lead to blindness
monogenic disorder causes by point mutations in single gene
(>60 causal genes identified in 2013)
causes erosion of the (peripheral) retina and release of photopigment from the photoreceptor cells
Rod death causes cascade effect for surrounding tissue
What is the rate of light response we can see?
can see a stimulus that is flickering 70x per second
What is needed in order for outer segments to produce a very fast response to light?
- v. high metabolic rate
- supply of O2 and nutrients to produce ATP/GTP
much higher metabolic demand than the brain
How is higher resolution sampling supported in photoreceptor outer segments?
- dense packing into arranged hexagonal array
- hence why there are no capillary beds seen near the retina
- gaps between photoreceptors would create gaps in vision
Where is the choroid located in relation to the peripheral retina?
on top of the retinal pigment epithelium