Congenital sensory deprivation can lead to reorganization of the deprived cortical regions by another sensory system. Such cross-modal reorganization may either compete with or complement the "original" inputs to the deprived area after sensory restoration and can thus be either adverse or beneficial for sensory restoration. In congenital deafness, a previous inactivation study documented that supranormal visual behavior was mediated by higher-order auditory fields in congenitally deaf cats (CDCs). However, both the auditory responsiveness of "deaf" higherorder fields and interactions between the reorganized and the original sensory input remain unknown. Here, we studied a higher-order auditory field responsible for the supranormal visual function in CDCs, the auditory dorsal zone (DZ). Hearing cats and visual cortical areas served as a control. Using mapping with microelectrode arrays, we demonstrate spatially scattered visual (cross-modal) responsiveness in the DZ, but show that this did not interfere substantially with robust auditory responsiveness elicited through cochlear implants. Visually responsive and auditory-responsive neurons in the deaf auditory cortex formed two distinct populations that did not show bimodal interactions. Therefore, cross-modal plasticity in the deaf higher-order auditory cortex had limited effects on auditory inputs. The moderate number of scattered cross-modally responsive neurons could be the consequence of exuberant connections formed during development that were not pruned postnatally in deaf cats. Although juvenile brain circuits are modified extensively by experience, the main driving input to the cross-modally (visually) reorganized higher-order auditory cortex remained auditory in congenital deafness.
General anesthesia is not a uniform state of the brain. Ongoing activity differs between light and deep anesthesia and cortical response properties are modulated in dependence of anesthetic dosage. We investigated how anesthesia level affects cross-modal interactions in primary sensory cortex. To examine this, we continuously measured the effects of visual and auditory stimulation during increasing and decreasing isoflurane level in the mouse visual cortex and the subiculum (from baseline at 0.7 to 2.5 vol % and reverse). Auditory evoked burst activity occurred in visual cortex after a transition during increase of anesthesia level. At the same time, auditory and visual evoked bursts occurred in the subiculum, even though the subiculum was unresponsive to both stimuli previous to the transition. This altered sensory excitability was linked to the presence of burst suppression activity in cortex, and to a regular slow burst suppression rhythm (∼0.2 Hz) in the subiculum. The effect disappeared during return to light anesthesia. The results show that pseudo-heteromodal sensory burst responses can appear in brain structures as an effect of an anesthesia induced state change.
The theory of predictive coding assumes that higher-order representations influence lower-order representations by generating predictions about sensory input. In congenital deafness, one identified dysfunction is a reduced activation of deep layers in the auditory cortex. Since these layers play a central role for processing top-down influences, congenital deafness might interfere with the integration of top-down and bottom-up information flow. Studies in humans suggest more deficits in higher-order than in primary cortical areas in congenital deafness. That opens up the question how well neurons in higher-order areas can be activated by the input through the deprived auditory pathway after restoration of hearing with cochlear implants. Further it is unclear whether their interconnections to lower order areas are impaired by absence of hearing. Corticocortical anatomical fiber tracts and general auditory responsiveness in both primary and higher-order areas are generally preserved in absence of auditory experience. However, the existing data suggest a dichotomy between preservation of anatomical cortical connectivity in congenital deafness and functional deficits in corticocortical coupling. Further, cross-modal reorganization observed in congenital deafness in specific cortical areas appears to be established by functional synaptic changes and rests on anatomically preserved, genetically-predetermined and molecularly patterned circuitry connecting the sensory systems. Current data indicate a reduced corticocortical functional coupling between cortical auditory areas in congenital deafness, both in bottom-up and top-down information stream. Consequently, congenital deafness is likely to result in a deficit in predictive coding that affects learning ability after late cochlear implantation.
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