Visual Plasticity Flashcards
Lazy eye is a…?
developmental issue
LGN input to…?
the primary visual cortex and OD columns
OD column development
- before birth, the retinae produce waves of synchronous activity that drive the cortical cells well
- after birth visual input drives co-ordinated retinal activity
- the afferents from each eye fire together independently of the other eye
- LTP!!!
- Receptors: NMDA receptors with Ca2+ and Mg
- synapses are strengthened or weakened depending on the relative amount of input from each eye
- The OD columns will segregate in response to this activity
Why is developmental plasticity important?
to treat amblyopia
what is amblyopia
- Amblyopia - lazy eye
- ptosis or cataract
OD columns and monocular deprivation in monkeys
- if one eye is compromised in early life then the brain makes very few connections with it ⇒ amblyopia
- an eye that may be functional yet has very poor acuity
- acuity even with optional correction
OD columns and monocular deprivation
- Cortical cells strongly and consistently driven by this eye (Left)
- cortical cells are not driven by this eye (right)
- Normally - afferents fire together in response to visual stimuli
- eye is compromised at birth - unconditional spontaneous activity only
- good eye - has access to abundant cortical machinery
- bad eye - little access to the cortical machinery hence image cannot be processed in detail
Can OD column shift be reversed? provide evidence
- Patching the good eye - forcing to actively work with bad eye
- might shift OD columns around if done EARLY enough but with the danger of compromising vision in the good eye and reducing stereoscopic vision
- 2 lines snellan chart improvement has been shown with on average ~ 170hrs total @ 4yo and >200hrs @ 6yo
OD can be tested physiologically by?
-recording from cells in layer 4C the input layer
-after early deprivation in monkey the great majority of ells are driven by non-deprived eye
-later deprivation doesn’t case a shift in dominance
Developmental plasticity is confined to a ‘critical period’
1w to 12w
the critical period for MD
first 10w of life
OD pattern becomes fixed at this point
What is the best option?
PREVENTION
-effects of MD develop rapidly but not simply reversible
all these may develop AY
- ptosis
- cataract
- strabismus
- anisometropia
can AY occur without a shift in OD columns?
-strabismic AY = lost bad eye late in life due to lost territory
-anisometropic AY = lost good eye late in life not due to lost territory
What is the mechanisms for non-MD AY?
OD cells recorder in PVC area V1
Plasticity in the intracortical circuits. Can be filling-in?
- Filling-in a scotoma of retinal origin
- Filling-in involves ectopic receptive fields
- Filling-in scotomas match their surroundings
- Filling-in involves expansion of receptive
- Filling-in invloves activation of existing connections
Other mechanisms?
a wave of axon sprouting and pruning is seen in the region of cortex affected by a new retinal lesion
-fMRI as evidence
The story so far
- The geniculocortical wiring fixes at the end of the critical period but intracortical wiring doesn’t:
- many silent cortico-cortical connections exist which play a role in normal vision
- these connections can be revealed in the short system and their synapses are likely capable of plasticity
- axons may remain capable of growth and retractions changing connectivity
- Hence grey matter circuits can change dramatically even in adult
Can adult plasticity be used to restore vision in AY?
- Perceptual learning and AY
- results for intensive training in detecting vernier offsets by amblyopic adults with good eye patched
- multiple ~1hr session
- sig improvemets seen
- fairly task specific e.g. maximal for the trained orientation
- but it improved snellen acuity too (20/80 → 20/22 vision)
- adult visual performance can be improved simply through practice
- training can improve performance of an amblyopic eye
- likely to be truly effective for strabismic / anisometropic amblyopia
Plasticity can be enhanced in adults. HOW?
-AY can be improved by reactivating ‘plasticity genes’
