Cortical plasticity in the face of congenitally altered input into V1.

Delineating the extent and limits of cortical plasticity is fundamental to understanding human neurophysiology. While cortical plasticity is often studied in the extreme cases of sensory loss (Büchel et al., 1998) or deafferentation (Buonomano andMerzenich, 1998), nature provides rare cases in which all ‘components’ of a neural network are intact, yet neural pathways develop atypically. Here we study such a case: the congenitally altered visual input into V1 present in albinism (Fig. 1a). In humanswith albinism, on average themost central 8 of the temporal retina decussates atypically to the opposite hemisphere at the optic chiasm (Hoffmann et al., 2005). Hence, for this portion of the visual field (VF) the lateral geniculate nucleus (LGN) does not comprise the usual maps of the contralateral VF, representing input from both eyes. Instead, it comprises maps of the contralateral and ipsilateral VFs, representing the sole input from the contralateral eye. Consequently, the corresponding primary visual cortex is deprived of binocular input and instead receives input from both VFs. Direct evidence from a non-human albinotic primate demonstrates that the normal ocular dominance arrangement gives way to a hemifield column arrangement (Guillery et al., 1984). Accordingly, in humans with albinism, the atypically routed ipsilateral and the typically routed contralateral representations are organized as retinotopic overlays, such that VF positions that are mirror-symmetrical along the vertical meridian are represented in close cortical vicinity to each other (Hoffmann et al., 2003). This organizational pattern, termed true albino pattern (Guillery, 1986), is due to a conservative geniculo-striate projection in albinism. As a result, the plasticity of the intracortical architecture is