Abstract:
Parvalbumin-expressing (PV) interneurons are known to play key roles in the inhibiton of pyramidal neurons in the auditory cortex of the brain, but little is known about the exact circuits they function in. The auditory cortex is associated with complex temporal processing tasks and emotional learning. Dysfunctions in the auditory cortex are a major cause of age-related hearing loss. Gap detection, a task that requires the auditory cortex, involves detecting short gaps in noise. This study looks to see how PV neurons respond during gap detection before and after fear conditioning in order to determine the role of PV cells in a circuit. We identified PV neurons in optogenetically engineered mice and recorded their activity during a gap detection test. The mice were given a fear conditioning learning program, then their neural activity was recorded as they performed the gap detection test again. We found that the majority of the mice did not improve at gap detection after fear conditioning. Additionally, the PV responses did not change with fear conditioning. We did see that mice with greater PV activity (larger gap termination responses) were more likely to improve at gap detection than mice with less PV activity. We conclude that larger gap termination responses are an indicator of worse gap detection. More research on PV cells is necessary to understand the relationship between gap detection and the GTRs of PV cells in the auditory cortex. A great understanding of these mechanisms could lead to potential treatments for those with hearing loss due to central auditory dysfunctions.