Amblyopia is a developmental disorder resulting in poor vision in one eye. The 
mechanism by which input to the affected eye is prevented from reaching the 
level of awareness remains poorly understood. We recorded simultaneously from 
large populations of neurons in the supragranular layers of areas V1 and V2 in 6 
macaques that were made amblyopic by rearing with artificial strabismus or 
anisometropia, and 1 normally reared control. In agreement with previous 
reports, we found that cortical neuronal signals driven through the amblyopic 
eyes were reduced, and that cortical neurons were on average more strongly 
driven by the non-amblyopic than by the amblyopic eyes. We analyzed multiunit 
recordings using standard population decoding methods, and found that visual 
signals from the amblyopic eye, while weakened, were not degraded enough to 
explain the behavioral deficits. Thus additional losses must arise in downstream 
processing. We tested the idea that under monocular viewing conditions, only 
signals from neurons dominated by - rather than driven by - the open eye might 
be used. This reduces the proportion of neuronal signals available from the 
amblyopic eye, and amplifies the interocular difference observed at the level of 
single neurons. We conclude that amblyopia might arise in part from degradation 
in the neuronal signals from the amblyopic eye, and in part from a reduction in 
the number of signals processed by downstream areas.