9/13 VisualSystem1 - Woodbury Flashcards
visual system processing
- light reflects off object, enters eye, gets focused on retina
- retina converts light image to neural signal
* central retina has more cells → more visual acuity - signal is compressed before leaving eye
- eye → optic nerve → optic tract → optic radiations → primary visual cortex
- implication: visual cortex takes best guess at a degraded signal, which is why sometimes what we see is not what actually is
what do we mean when we say the human retina is “inverted”?
why?
what are the consequences?
light comes through lens, but has to pass through upper layers (where light is reflected, sbsorbed, altered) before finally getting to outer segment where the photoreceptors are
potential explanation: protection
- we are exposed to a lot of light
- light generates heat
- huge blood supply in choroid under RPEs that conducts this heat away
consequence: visual acuity is compromised!
exceptions to the general “inverted design” of retina
- fovea : site of best vision
- optic disc : blind spot
how do photoreceptors respond to light?
in dark, cells are DEPOLARIZED (“dark current”)
- glutamate nt release is maximal
in light, cells are HYPERPOLARIZED (no dark current)
- nt release diminished
graded response!
no action potentials generated. instead, amt of glutamate is a signal for the presence of light AND its intensity
specifics of photoreceptor response to light
receptors involved and responses to dark/light
outer segment contains…
- cGMP-gated channels
- cGMP present → channels open, Na flows in
- regulated by light
-
K pump → K pumped out
* constitutively on
in the dark, Na inflow > K efflux → cell depolarized, glutamate increased
in light, cGMP drops/Na channels close, such that Na inflow < K efflux → cell hyperpolarized, glutamate decreased
opsin
receptor
what happens when the receptor is activated? basic
prototype photopigment
- 7 TMD G-protein-linked receptor
- absorb light, initiate signaling cascade that leads to cGMP drop → hyperpol
rods and each cone type have diff types of opsin
receptor = opsin + vitA derivative cis-retinal
- light converts cis-retinal → trans-retinal (low affinity for opsin)
- trans-retinal dissociates from opsin, causing receptor to change conformation → interaction with G protein (transducin) occurs, starting cascade
- activated receptor interacts with transducin (normally kept inactive by inhibitors)
- activated transducin interacts with PDE (phosphodiesterase) (normally kept inactive by inhibitory subunits)
- activated PDE cleaves cGMP!!!! → inactivates cGMP and reduces its levels
why does cGMP drop in response to light?
detailed
- intro: light hits photoreceptor, which contains opsin + cis-retinal → converts cis to trans, activating receptor!*
- activated receptor interacts with transducin (normally kept inactive by inhibitors)
- intro: light hits photoreceptor, which contains opsin + cis-retinal → converts cis to trans, activating receptor!*
- GDP → GTP knocks off inhibitors of transducin, activating it
- receptor stays active for a while, can activate more transducins → signal amplification possible
- activated transducin interacts with PDE (phosphodiesterase) (normally kept inactive by inhibitory subunits)
* transducin removes inhibitor from one or both PDEs → PDE activated - PDE cleaves cGMP!!!! → inactivates cGMP and reduces its levels
light → closed Na influx channels
steps in the cascade
light
→ activates receptor
→ activates transducin
→ activates PDE
→ inactivates cGMP
→ closes cGMP-gated Na influx channels
PDE inhibitors adverse effects!
Viagra = PDE inhibitor → can affect vision!
getting info from photoreceptors to optic nerve
whats the path?
whats the problem?
who “solves” it?
100M photoreceptor cells in outer nuclear layer → 1M retinal ganglion cells (which will coalesce to form optic nerve)
problem: info has to be compressed somehow!
- signal compression happens in inner nuclear layer
- inner nuclear system prioritizes info the decide what has to be kept and what gets tossed
- EDGES (define the object)
- other details
- visual cortex takes its best guess to fill in the details lost during compression
cell types involved in signal compression
all found in inner nuclear layer
1. bipolar cells (most abundant)
- vertical transmission (sends signals up chain)
- graded response
- no APs
- uses glutamate
- miminal signal compression
- up to 50rods:1, 5cones:1, but these ratios only hold in peripheral retina
2. horizontal cells
- lateral inhibition
- most cases: inhibit photoreceptor hyperpol and bipolar response, allow edge info to pass through
- primary point of signal compression
3. amacrine cells (similar to horiz cells; worse understood)
- also lateral inhibition
- operate at inner plexiform layer (between bipolar cells and RGCs)
- second filter to reassess what horizontal cells let through
center-surround receptive field
when you stimulate a large area of retina → minimal response
- activating surrounding photoreceptors inhibits RGC response bc you’re no longer defining an edge
center and surround areas oppose one another
- stim center only: incr firing
- stim center/surround: slight incr firing
- stim surround only: decr firing - volley when stim removed
cell specific responses to…
center only stim
center/surround stim
surround only stim
center only stim = defining an edge
- horizontal don’t intervere
- bipolar signals
- RGC fires volley
center/surround stim = not defining an edge
- horizontal intervere
- bipolar blocked
- RGC fires around background level
surround only stim = defining an edge
- horizontal don’t intervere
- bipolar signals
- RGC fires volley
classes of RGCs
1. M cell (‘motion’)
- large receptive fields
- large caliber axons
- carry info to motion detectors
- can’t detect motion themselves, but relay to cells that can in visual cortex
2. P cells (‘precision’)
- small receptive fields
- small caliber axons
- carry info re: form/shape
areas of the retina that are “different”
- macula (incl fovea)
- optic disc
consequences of lesions at diff points
