It has been 25 years since the seminal work of Rauschecker and Korte that essentially forged the field of crossmodal plasticity. Since then, a great deal has been learned about the mechanisms of neuronal plasticity that have brought into question some of the popularly held notions derived from this classical work. Specifically, crossmodal plasticity has also become synonymous with ‘adaptive’ or ‘compensatory’ plasticity, but recent work from Steve Lomber’s lab has shown that only a subset of modality-specific processing features may be augmented by this process, and evidence from Alex Meredith’s lab shows that some crossmodal effects may even be maladaptive. Similarly, it has been asserted that crossmodal plasticity is the pervue of the cerebral cortex, but the work of Susan Shores’ group has now demonstrated crossmodal reorganization at multiple sites in the brainstem. Furthermore, although the effects of crossmodal plasticity are largely manifest after early sensory lesions, Brian Allman has shown that massive crossmodal reorganization of auditory cortex occurs following deafening in adult animals. These conceptual shifts have clinical relevance: given that hearing impairment in adults is among the most prevalent neurological disorders in man, these data indicate that crossmodal plasticity could play a profound role in sensory perception and disorders in a very large number of individuals. Therefore, it is an appropriate time to re-evaluate the fundamental issues of crossmodal plasticity, but with respect for that which has brought the field to this point.

Susan E Shore, Ph.D.
Kresge Hearing Research Institute,
University of Michigan Medical School

A feature of multisensory neurons is their capacity for crossmodal innervation following sensory deprivation. Multisensory neurons in the dorsal cochlear nucleus receive auditory input via VIIIth nerve fibers as well as somatosensory input via the axons of cochlear nucleus granule cells. This pattern of convergence would suggest that reduction of VIIIth nerve input to the cochlear nucleus would result in compensatory innervation via the somatosensory input systems, one of which is trigeminal. Comparison of DCN responses to trigeminal and bimodal (trigeminal plus acoustic) stimulation in normal and noise-damaged guinea pigs showed that the latter had significantly lower thresholds, shorter latencies and durations, and increased amplitudes of response to trigeminal stimulation than normal animals. Noise-damaged animals also showed a greater proportion of inhibitory and a smaller proportion of excitatory responses compared with normal. The number of cells exhibiting bimodal integration, as well as the degree of integration, was increased after noise damage. These results indicate that projections from the trigeminal system to the cochlear nucleus are amplified and reorganized after hearing loss, and point to crossmodal reorganization of this major brainstem sensory nucleus.

Brian Allman, Ph.D.
Virginia Commonwealth University

Crossmodal reorganization, a phenomenon whereby the responsiveness of a sensory area is converted from a deprived modality to that of an intact sensory system, commonly occurs in response to developmental lesions. However, little is known about its capacity for crossmodal remodeling in the adult brain. In this context, the potential for cortical crossmodal reorganization was examined in ferrets deafened as adults. Recordings from adult-deafened ‘auditory’ cortex revealed an extensive conversion: neurons once activated by auditory cues were now driven by somatosensory stimulation. This effect was observed within 16 days of deafness. Recordings from hearing animals indicated that subthreshold somatosensory inputs were insufficient for their unmasking, by deafness, to account for the observed conversion. Lack of change in anatomical connectivity suggests that the crossmodal conversion may be reflective of reorganization elsewhere in the auditory pathway, such as has been demonstrated in the brainstem of hearing impaired animals. Collectively, these data demonstrate that significant cortical crossmodal reorganization can occur after the period of sensory system maturation has ended.

Stephen G. Lomber, Ph.D.
Centre for Brain and Mind
University of Western Ontario

When the brain is deprived of input from one sensory modality, it often compensates with supernormal performance in one or more of the intact sensory systems. In the absence of acoustic input, it has been proposed that “deaf� auditory cortex may be recruited to perform visual functions. To test this hypothesis we examined the visual capabilities of congenitally deaf cats (and hearing controls) on a battery of visual tasks to define which visual abilities are affected by cross-modal compensation. For tests of grating acuity, Vernier acuity, direction of motion discrimination, velocity discrimination, and orientation discrimination performance in the deaf cats was similar to that of hearing cats. However, for two tests (movement detection and localization of a flashed stimulus) the deaf cats demonstrated superior performance to that of the hearing cats. To determine if crossmodal reorganization in auditory cortex contributes to the superior visual capabilities of deaf cats, we bilaterally placed cooling loops on A1, DZ, AAF, and PAF to permit their individual deactivation. Deactivation of neither A1, nor AAF, altered performance on either the movement detection or visual localization tasks. However, bilateral deactivation of PAF resulted in the elimination of the superior visual localization capabilities of the deaf cats and resulted in performance similar to hearing cats. Furthermore, bilateral deactivation of DZ resulted in the elimination of the superior movement detection capabilities of the deaf cats and resulted in performance similar to hearing cats. Therefore, the results demonstrate a double dissociation, with superior visual localization abilities mediated by PAF and superior movement detection abilities mediated by DZ. These observations demonstrate that enhanced visual performance in deaf cats is caused by cross-modal reorganization within “deaf� auditory cortex and that it is possible to localize and dissociate individual visual functions within reorganized auditory cortex.


Gary D. Paige

Department of Neurobiology & Anatomy, Center for Navigation & Communication Sciences, and Center for Visual Science, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642 USA

Optical prisms shift visual space and induce a gradual adaptive realignment of various sensory-motor reference frames. In humans, one form of prism-adaptation is a shift in sound localization. However, we recently reported that sustained eccentric eye position alone also shifts sound localization, approaching ~40% of ocular eccentricity over several minutes and in the same direction. We surmised that prism adaptation may well reflect contributions of both eye position and cross-sensory plasticity. Specifically, given a prismatic shift of the visual world, eye position must also shift to fixate the same field of targets. Over time, this average bias of eye position, apart from potential cross-sensory plasticity, may cause a corresponding shift in sound localization. Our new findings support the notion that prism adaptation of auditory space depends upon two influences: 1) the effect of displaced mean eye position induced by the prisms, which occurs early and without cross-sensory spatial experience (diotic and near-deafness conditions); and 2) a more gradual and experience-dependent cross-sensory learning in response to an imposed offset between auditory and visual space, which augments the eye position effect under natural binaural conditions. These mechanisms act synergistically in cross-modal adaptation to spatial disparity imposed by optical prisms.