Our understanding of the physiological basis for amblyopia in humans h
as undergone dramatic changes over the past two decades. The first suc
h change occurred when we were first able to record from single neuron
es in different parts of the visual pathway and develop neural models
of the anomaly. The second came from psychophysical investigations and
evaluations of these animal models. Our understanding has progressed
from one focused on the properties of single cortical cells to an appr
eciation of the anomalous behaviour of cellular networks.