9/13 VisualSystem1 - Woodbury Flashcards Preview

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Flashcards in 9/13 VisualSystem1 - Woodbury Deck (25)

visual system processing

1. light reflects off object, enters eye, gets focused on retina

2. retina converts light image to neural signal

  • central retina has more cells → more visual acuity

3. 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"?


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

1. fovea : site of best vision

2. 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...

1. cGMP-gated channels

  • cGMP present → channels open, Na flows in
  • regulated by light

2. 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






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


1. activated receptor interacts with transducin (normally kept inactive by inhibitors)

2. activated transducin interacts with PDE (phosphodiesterase) (normally kept inactive by inhibitory subunits)

3. activated PDE cleaves cGMP!!!! → inactivates cGMP and reduces its levels


why does cGMP drop in response to light?


1. intro: light hits photoreceptor, which contains opsin + cis-retinal → converts cis to trans, activating receptor!

2. activated receptor interacts with transducin (normally kept inactive by inhibitors)

  • GDP → GTP knocks off inhibitors of transducin, activating it
  • receptor stays active for a while, can activate more transducins → signal amplification possible

3. activated transducin interacts with PDE (phosphodiesterase) (normally kept inactive by inhibitory subunits)

  • transducin removes inhibitor from one or both PDEs → PDE activated

4. PDE cleaves cGMP!!!! → inactivates cGMP and reduces its levels


light → closed Na influx channels

steps in the cascade


→ 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"

  1. macula (incl fovea)
  2. optic disc


what's special about the fovea

area of best vision

  • intervening layers between light and photoreceptors are pushed aside for a direct route
  • only cones present
  • v high density of cells


what is the macula?

region of high visual acuity surrounding/including the fovea

  • macular degen damages this area → loss of central vision


optic disc

"blind spot"

  • axons from RGCs coalesce and exit through optic disc
  • blood vessels enter eye at optic disc

→→→ no photoreceptors in this area = no vision!


optic nerve


diff between M cells and P cells pertaining to optic nerve

M cells have larger axons → faster signal transduction

M cell signals get to brain faster than P cell signals do


visual information from one side of the body is received in both eyes (temporal and nasal fields)

ex. image on left is received in L nasal and R temporal fields


how do we get info onto the correct side of the brain?

40% of visual info is already on correct side

rest of it travels via partial decussation at optic chiasm (no synapse! just crossing over)

  • optic chiasm splits things into optic nerve (anterior to chiasm) and optic tract (posterior to chiasm)
  • most axons (90%) will travel to Lateral Geniculate Nucleus (LGN; part of thalamus)
  • other 10% goes to other areas
    • suprachiasmatic nucleus (circadian rhythms through pineal)
    • pretectum nucleus (pupillary light reflex)
    • superior colliculus (eye movements; coordinate vision with other senses)


lateral geniculate nucleus


layers: which axons go where, special input features of layers

6 layered nucleus that receives input from optic tracts

  • axons from both eyes are mixed in optic tracts
  • each layer of LGN receives axons from only one eye (re-segregate)

mnemonic: see I? I see, I see = ciicic = 123456

[layer1 is inside curve, layer6 is outside curve; c=contralat, i=ipsilat]


layers 1 and 2 (magnocellular cells) get input from M cells

  • "magnocellular advantage"

layers 3-6 (parvocellular) get input from P cells


evolutionarily...magnocellular levels have prob been around for longer (motion) than parvocellular cells (discrimination)


magnocellular advantage

info re: motion (on M cells) gets to visual cortex faster!

  • big axons (M cells) synapsing on cells with big axons in LGN

might be imp for reading → keeping fovea focused on text


effects of glaucoma at LGN

LGN neurons die if they lose their input

  • this is where 1-6 ciicic comes into play! can use to determine which layers of LGN will be affected by a glaucoma (or vice versa)


how to get from LGN to final destination

LGN → optic radiations → calcarine sulcus


optic radiations have 2 divisions

  1. superior retina (inf visual field) → upper banks of calcarine
  2. inferior retina (sup visual field) → lower bank of calcarine
    • travel through Meyer's Loop, extend forward in temporal lobe
    • more susceptible to damage! bc travel further more superficially

calcarine sulcus houses primary visual cortex aka V1 aka striate cortex


consequences of lesions at diff points

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