In primates, visual function is dominated by the pathway that transmits visual information from the retina, via the lateral geniculate nucleus (LGN), to the primary visual cortex (V1). Although lesions of V1 lead to blindness, it is well documented that residual visual function can be retained within scotomas caused by V1 lesions, including (largely subconscious) abilities to locate some types of stimuli, and even to coarsely evaluate their characteristics (“blindsight”). These observations indicate that other thalamic projections can convey retinal inputs directly to the extrastriate cortex, bypassing V1. The exact characteristics of blindsight depend markedly on the age at which the lesion occurs. Patients and monkeys who sustained lesions early in life often show a greater range of abilities than those who had lesions in adulthood, including, in many cases, conscious perception. My laboratory has been investigating the types of physiological changes in subcortical and cortical areas which mediate such outcomes. For this purpose, we have developed a V1 lesion model based on the marmoset monkey, a small new world primate in which the anatomy and physiology of the visual pathways has been well characterised, and has accelerated development in comparison with macaque monkeys. In this talk, I will briefly review the characteristics of the marmoset as an advantageous animal model for studies of primate vision, including plasticity, describe recent findings on the physiological consequences of V1 lesions at different ages, and briefly report on current lines of work aimed at understanding the full circuitry of the marmoset visual cortex using a neuroinformatics approach.