Masters of Clinical Anatomy Projects
It is well established that high-intensity noise exposure can induce structural and physiological changes in the primary auditory cortex, such as impaired GABA neurotransmission, which leads to a reduced level of GABA-synthesizing enzymes (i.e., GAD65/67). At present, however, it remains unknown how partial hearing loss affects GABA neurotransmission in areas of the cortex that process sound as well as other sensory modalities (e.g., visual stimuli). In the present study, we are using a rat model to investigate our working hypothesis that noise-induced hearing loss causes a differential effect on GAD67 levels in the various cortical areas capable of sound processing, such that the multisensory cortex will not show the same dramatic reduction as in the primary auditory cortex. Adult male rats were exposed to loud noise (0.8-20 kHz at 120 dB SPL for 2h), which caused a 27 ± 9 dB elevation of their hearing threshold 14 days following the noise exposure. Using immunohistochemistry, the level of GAD67 was compared between noise-exposed rats and age-matched controls in multiple auditory, visual and multisensory cortical areas. Consistent with our hypothesis, preliminary findings suggest that the multisensory cortex does not experience the same degree of impaired GABA neurotransmission as the primary auditory cortex following noise-induced hearing loss.