Fig. 4: Suggested mechanism of dynamic crossmodal plasticity.

In a hearing auditory cortex (A), the heteromodal inputs are only modulatory and are therefore dependent on the driving auditory input. Provided this is present, the responses can be significantly modified by heteromodal inputs. In hearing loss (B), there is reduced or no driving input and thus homeostatic plasticity may increase excitability to such an extent that the previously weak modulating input becomes driving. Thereby both the heteromodal response and neuronal sensitivity increase, i.e. the spiking thresholds to an input is decreasing. After hearing restoration (C), the gain is reduced due to the restoration of a strong driving input. The heteromodal input becomes modulating again. Since hearing restoration is rarely complete, the gain of cortical neurons is in between the one of deaf and hearing subjects. In the illustrated schematics, the changes are modeled only by an effect on spiking threshold and response increase. This is a simplification of the multiplicity of homeostatic processes present physiologically.