08

Question 1

Two things blamed to describe amblyopic vision loss?
-which explains the changes seen in a monkey reared in the dark for 4 months?

-does their loss occur @ the level of the visual cortex?

Answer 1

misuse, lateral inhibition

• MISUSE does - there is no lateral inhibition when BOTH eyes see nothing (in the dark for 4 months)
• NO

Question 2

Do the losses seen in the monkey 3-4 weeks after exposure to light occur in the visual cortex?

-Where DO they occur? To what severity (modest, severe ,etc.)

Answer 2

NO - just know that

Area 19 (V4, V5) - primary input from senses - MODEST loss that recovers quickly w/ exposure to light

Area 7 - posterior temporal - multisensory input (reaching/grasping/motor circuitry input) - SEVERE loss - ALSO recovers w/ onset of visual experience

Question 3

Loss in the striate cortex (primary visual system) is induced by what amblyopic mechanism?
-What about loss in the multisensory (area 7) areas? What type of inhibition induces those changes?

Answer 3

striate cortex loss - lateral inhibition
multisensory area loss - intersensory inhibition - visual input was inhibited by input of other senses - RECOVERS with visual experience

Question 4

T/F: In a dark reared monkey, the critical period is triggered immediately.

Answer 4

FALSE - critical period is only triggered upon exposure to LIGHT!
-important: primary visual system remains NORMAL and ready to recover with visual experience

Question 5

T/F:
-A binocularly form-deprived monkey show losses in the CSF in both eyes

-A MONOcularly form-deprived monkey shows CSF losses in the deprived eye. What’s the cause here?

Answer 5

-FALSE - LITTLE/NO LOSS in both eyes (one may have moderate loss, but that’s it)

• TRUE - SEVERE losses in the monocularly-deprived eye.
  
  • cause: interocular inhibition in the ocular dominance columns

Question 6

What’s the most extreme form of amblyo? What are the two main areas affected?

Answer 6

Monocular deprivation amblyopia. 1) LGN, 2) Striate cortex

Question 7

Monocular form dep - affects LGN and Striate Cortex. Name the main changes seen in each area.

Answer 7

LGN: 1) lack of neuron growth in layers of the deprived eye, 2) HIGH CS loss in the PARVO (X) cells in the CENTRAL VF of the deprived eye

Striate Cortex: 1) thinner oc. dominance columns for the deprived eye, 2) cortical UNRESPONSIVENESS to the deprived eye

Question 8

In the LGN of a monocularly form-deprived eye, high frequency CS loss is seen in which cells? In what area of the VF?

• is any other area of the VF affected?
• T/F: neurons grow normally in the BINOcular parts of the VF

Answer 8

high CSF loss in the PARVO cells of the CENTRAL (15-20) deg of the VF

• it’s NOT affected in any other area
• FALSE: the DON’T grow normally - lack of growth is d/t interocular inhibition - monocular growth is normal!

Question 9

T/F: deprivation of growth in BINOcular parts of the VF occurs in all types of amblyopia

Answer 9

FALSE - only true for form deprivation!

Question 10

In the striate cortex, THINNING of the oc dominance columns occurs at about what percentage?
-this change is d/t what?

Answer 10

60/40%

-d/t CORTICAL UNRESPONSIVENESS in all layers of the deprived eye, d/t ASYMMETRIC PRUNING BACK

Question 11

Even though it’s only a 60/40 change in the striate cortex, what impact does HABITUATION and SENSITIZATION play in creating such a dramatic change?

Answer 11

Habituation: neuron loses axon terminals (it’s used to receiving less information)
Sensitization: neurons stimulated more send out more side shoots/have more synaptic connections - increases its input, AND increases INHIBITORY input over the amblyopic eye (exacerbates problem)

Question 12

What’s the first change to occur in monocularly deprived cats and monkeys?

Answer 12

cortical neurons STOP RESPONDING to the deprived eye

Question 13

If a human eye is enucleated during infancy, what happens? What ends up being even BETTER than in normals?

Answer 13

more cortex is taken over by the intact eye - increase VA, CSF, HYPERACUITY - even better than in nmls!

Question 14

Critical period begins when?

• in lower animals, what’s the limiting factor?
• in monkeys/humans, what’s the limiting factor?

Answer 14

retinal illumination occurs - critical period starts - both ACTIVATES AND CREATES cells that will provide inhibition to guide development

lower - neuromodulator release
higher (humans) - neuromodulators sero/NE already released, just waiting for RETINAL ILLUMINATION

Question 15

GABA - the great inhibitor

• levels (increase/decrease) as you age? Why?
• what happens when there is EXCESS GABA? How is this affected by Prozac?

Answer 15

• INCREASE w/ age - slows the critical period, limits recovery from damage - still allows some learning/adaptation
• Excess = over-inhibition - reduces overall plasticity - makes recovery from amblyo more difficult - happens in Down’s, Rett syndrome
• Prozac: inhibits the inhibitor - in animals studies, has allowed more plasticity in the system well after the critical period

Question 16

When does the critical period end?

Answer 16

when nonspecific inputs decrease, and NMDA receptors are altered - some are more plastic than others

Question 17

What are the three types of NMDA receptors? Which are more plastic/stable?

Answer 17

NR1: decrease in cortex during first 6yrs of life - VERY plastic
Nr2b: decrease in first 3yrs of life - VERY plastic
Nr2a: INCREASE up to 6yrs - LESS plastic (more stable) (A’s are stAble)

Question 18

Expected result w/

• Full-time patching:
• NO patching:
• Half-time patching

Answer 18

Full: fast VA recovery, then immediate REGRESSION (in BOTH eyes - but the good eye recovers)

No patching: slow recovery of amblyopic, only partial recovery

Half-time patching: (3.5-5hrs) - good eye sees better during therapy, but VA continues to improve AFTER patching d/c’d altogether - eventually gets to NORMAL in both eyes!

Question 19

Recovery in form-deprivation:

• 1) if eye is opened after critical period:
  2) if eyes is opened after critical period and other eye is patched:
  3) does recovery occur faster/more completely with earlier or later patching?

Answer 19

1) NO recovery
2) recovery
3) yes. this is obvious.

Question 20

Patching in ANISOmetropic amblyos causes the critical period to end at what age?

-What about if you were to patch AND incorporate vision therapy?

Answer 20

18 years

300 yrs - so, indefinitely if vision training included

Question 21

Cynader and Stryker looked at ___ cell size
-Conclusion: if you patch one eye for the first 6 months, then patch the GOOD eye for the next 6 months, what will result?

Answer 21

LGN

• almost total recovery in the LGN cell size - the initial cells that didn’t grow grew back, and equalled out to being back to normal
• take-home: CAN alter the critical period recovery time if you’re persistent enough

Question 22

Dews and Wiesel looked at __/visually guided motility

-Conclusion: if you wait to d/c patching until you’re way outside the critical period, what results?

Answer 22

VA

• good, but NOT COMPLETE, recovery of VA, but you DO get a FULL recovery of motility/motor behavior
• again, shows things are still happening outside the critical period

Question 23

Chow and Stewart included ____ training in the deprived eye after ~2yrs of deprivation.

-Significant changes after 1yr in sizes of LGN cells, oc. dominance columns (cortex) and behavior, but not as much of a change in ___ ___ responsiveness - VA didn’t improve by much

Answer 23

visual training

-visual cortex responsiveness - not much change - VA still improved after patching D/Cd, but not by as much as in other experiments

Question 24

Ganz and Haffner used horizontal and vertical lines to determine that cats use ____ instead of pattern discrimination to determine the orientation of the line

-take home?

Answer 24

flicker

-amblyopic subjects have tricks that allow them to do things, even if they aren’t using the mechanism you’re trying to test!

Question 25

Ganz et al discovered that interocular transfer (showing an animal to do a task with one eye only, then the other) - what happens in animals raised with alternating binocularity? What if these animals are amblyopic?

Answer 25

normal, under alternating occlusion - two independent visual systems - no sharing b/w cortical cells - no need to relearn task w/ separate eye b/c the code for pattern info from one eye is the same as the other

-amblyopic animals - must relearn task w/ each eye - pattern info coming from dominant eye is NOT the same pattern info as what’s coming from the amblyo eye.

Question 26

In amblyopic humans where the GOOD, non-amblyopic eye is enucleated, will vision in their bad eye return?
-Which type of acuity will show some improvement? Which type will not?

Answer 26

yes - some of it.

-resolution acuity will return (partially), but optotype acuity is slow to improve (b/c there’s a different code, remember? Requires RELEARNING)