Masters of Clinical Anatomy Projects
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 evaluated our hypothesis that this noise-induced crossmodal plasticity can also be assessed by mapping the expression of the activity marker, c-Fos, across multiple cortical areas in response to visual stimuli. Adult male rats were exposed to a 120dB noise (0.8-20kHz) for two hours, and the level of hearing loss was assessed with an auditory brainstem response (average hearing loss ~22±5 dB). Fourteen days later, noise-exposed rats (and age-matched shams) were subjected to a visual stimulation protocol known to induce c-Fos activation (200 light flashes; 1-3s ITI), followed by transcardial perfusion two hours post-stimulation. Visually-responsive neurons in the noise-exposed and sham rats were confirmed with immunohistochemistry and fluorescent microscopy. Inconsistent with our previous electrophysiological studies, the molecular mapping of c-Fos did not demonstrate an increased responsiveness to visual stimulation in the auditory and multisensory cortices following noise exposure. However, these results may be confounded by the short duration (6 min) of the visual stimulation protocol, as it evoked lower levels of c-Fos than previously reported in the literature. Future work will continue to investigate whether molecular mapping represents a useful tool for studying crossmodal plasticity.