Is territorial expansion a mechanism for crossmodal plasticity?

Crossmodal plasticity is the phenomenon whereby, following sensory damage or deprivation, the lost sensory function of a brain region is replaced by one of the remaining senses. One of several proposed mechanisms for this phenomenon involves the expansion of a more active brain region at the expense of another whose sensory inputs have been damaged or lost. This territorial expansion hypothesis was examined in the present study. The cat ectosylvian visual area (AEV) borders the auditory field of the anterior ectosylvian sulcus (FAES), which becomes visually reorganized in the early deaf. If this crossmodal effect in the FAES is due to the expansion of the adjoining AEV into the territory of the FAES after hearing loss, then the reorganized FAES should exhibit connectional features characteristic of the AEV. However, tracer injections revealed significantly different patterns of cortical connectivity between the AEV and the early deaf FAES, and substantial cytoarchitectonic and behavioral distinctions occur as well. Therefore, the crossmodal reorganization of the FAES cannot be mechanistically attributed to the expansion of the adjoining cortical territory of the AEV and an overwhelming number of recent studies now support unmasking of existing connections as the operative mechanism underlying crossmodal plasticity. Following sensory loss (e.g., deafness), a proposed mechanism underlying crossmodal plasticity is that the territory of a deprived brain region (area ‘A’) is taken over by neighboring, more active regions of the brain (enlarged area ‘B’ – bottom left). However, the present study determined that a crossmodally reorganized (‘Reorganized area A’) cortical region retains its areal distinctions (connectivity, cytoarchitectonics, and function – bottom right), which is not consistent with being incorporated (large X) into another area (area ‘B’).