Plasticity and stability of visual field maps in adult primary visual cortex

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Abstract
Reports over the past two decades suggest that adult primary visual cortex (V1), the dominant cortical relay station distributing visual sensory input to the rest of the neocortex, reorganizes substantially following sensory deprivation. This is an important claim because it suggests that the adult visual cortex retains significant potential for plasticity that might one day be harnessed to promote recovery after injury. It also means that the rest of the neocortex must be able to update its interpretation of V1 signals. We review the literature and point out several dissenting reports which suggest that adult reorganization in V1 is limited. We also describe some significant differences among the reports that claim reorganization does take place. For example, there are disputes about whether monocular or only homonymous binocular retinal lesions induce reorganization; about the effect of such lesions on receptive field size; about the time course of reorganization in response to retinal lesions; and about the extent of sub-cortical reorganization and its potential role in shaping cortical responses. We stress the need to resolve these important inconsistencies. An important deficiency in the literature is that measurements are often interpreted without the guidance of quantitative theory or closely coordinated behavioural measurements. No theory has emerged that integrates the measurements obtained using different modalities, from unit recording to neuroimaging to behaviour. Such a theory is needed, is possible and should be developed. Clarifying the extent of adult cortical plasticity under normal conditions, and the extent to which the cortex can be made plastic in response to injury or sensory deprivation, has implications for clinical applications and policy development. We conclude that at present the data do not support a strong position in favour of dynamic, large-scale reorganization of V1 responses. Rather, we argue that it is time to address the problem using new experimental and theoretical tools that measure, in vivo, specific cortical circuits and to understand the conditions under which specific neuronal pathways are plastic or stable.