Mapping Cortical Plasticity Following Noise Exposure Using c‐Fos Immunoreactivity

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Using in vivo electrophysiological recordings in rats, our lab has recently observed that high‐intensity noise exposure causes an increase in the number of neurons in the auditory and multisensory cortices that are responsive to visual stimuli (i.e., cortical crossmodal plasticity). To extend this work, the present study is evaluating our hypothesis that this noise‐induced crossmodal plasticity can also be assessed by mapping the activation of the immediate early gene, c‐Fos, across multiple cortical areas in response to visual stimuli. Adult male rats are exposed to a 120dB noise (0.8‐20kHz) for two hours, and the level of hearing loss is assessed with an auditory brainstem response (average hearing loss ~20dB). Fourteen days later, noise‐exposed rats (and age‐matched controls) were subjected to a visual stimulation protocol known to induce c‐Fos activation (200 light flashes; 1‐3 s ITI), followed by transcardial perfusion two hours post‐stimulation. Visually‐responsive neurons in the noise‐exposed rats and controls were confirmed with immunohistochemistry and fluorescent microscopy. If, as hypothesized, we observe an increase in the number of c‐Fos‐immunoreactive neurons in noise‐exposed rats, this would establish that molecular mapping represents a useful tool for studying cortical crossmodal plasticity.