PROJECT SUMMARY
Amblyopia is a disorder of spatial vision despite good retinal image quality and eye health. It affects 2-3% of
the population and almost always develops with early misalignment (strabismus) or unequal refractive power
(anisometropia), or form deprivation (cataract). Most studies on human amblyopia concentrate on thresholds
for contrast, size or offset, but striking perceptual distortions have been documented by asking amblyopes to
describe or draw clearly visible high-contrast letters, rings, and sinusoidal gratings. Form distortions are likely
to be at least as big a problem as loss of visual resolution for daily life. Forms are defined by local orientations,
and almost all neurons in primary visual cortex (V1) are tuned for orientation, highlighting its importance in
parsing visual images. The replicable systematic perceptual distortions of gratings drawn by amblyopes are
unexplainable with a neural scrambling model or a systematic shift in the neural map, but are compatible with
errors in the neural encoding of orientation in V1, while also involving decoding mechanisms in later cortical
areas. Our team of researchers and clinicians proposes to examine the neural development and functional
implications of the grating distortions by using our recent psychophysics, electrophysiology and modeling
results in the domains of ON/OFF system imbalance in amblyopia, cortical map formation, orientation
processing across V1, and the processing of parallel orientation signals for perceptions of 3-D shape, object
pose and mirror symmetry. We aim to model the neural development of errors in orientation encoding as a
consequence of ON-OFF imbalance caused by anisometropia and strabismus, which limits the orientation
tuning and spatial resolution of V1 neurons and shrinks the ocular dominance columns for the amblyopic eye.
We will also examine if orientation processing errors in the amblyopic eye make it difficult to do higher level
tasks that rely on orientation cues, or if there is some compensatory mechanism, and if the fellow eye performs
normally, overcompensates, or is handicapped because the lack of stereo makes it difficult to calibrate
monocular cues during development. Psychophysical and electrophysiological data suggest that amblyopia
also involves abnormalities in cortical areas after V1, suggesting that physiological changes may be
propagated and amplified in higher cortical areas that may have prolonged windows of plasticity. In addition,
regions of V1 that are unresponsive during passive viewing of visual stimuli in macular degeneration, can be
activated by engaging the subjects in a stimulus-related task, suggesting a role for top-down influences on
plasticity. The stimuli we use to identify deficits in functionally important visual tasks could be used to trigger
top-down signals from higher brain areas as part of the design of future treatments for recovery of perceptual
performance in adulthood, which would supplement treatments for improving visual acuity and binocularity.
Possibly the biggest payoff could come from directly testing if top-down signals from these tasks reactivate
plasticity in orientation selective V1 neurons in adult amblyopes.