Long-duration low-level (LDLL) noise exposures can enhance or depress sound-evoked activity in the auditory cortex (AC), but it?s unclear if these neuroplastic changes originate in the AC or are inherited from lower levels of the auditory pathway. To address this, recordings will be obtained from the cochlea, inferior colliculus (IC) and AC to determine the magnitude and direction of change. To determine if LDLL noise exposures disrupt the neural input to the central auditory pathway, we will evaluate the inner hair cell pre- synaptic ribbons and key proteins expressed on the post-synaptic type I afferent fibers. Our working hypothesis is LDLL noise exposure depresses the neural output of the cochlea, but the central auditory pathway compensates for this by enhancing neural gain at progressively higher levels of the auditory pathway.
Long-duration, low-level (LDLL) noise exposure can result in a temporary threshold shift and functional changes in central auditory structures. The goals of this project are to determine if LDLL noise: 1) alters inner hair cell pre-synaptic ribbons or post-synaptic receptors on type I auditory nerve fibers and 2) changes the neurophysiological gain (i.e., response amplitude) along the auditory pathway (cochlea, inferior colliculus and auditory cortex) to compensate for a diminished neural output from the cochlea. The proposed studies will provide novel insight on how prolonged exposure to low-level noise affects the peripheral and central auditory systems.
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