The cochlea adjusts sensitivity depending on the loudness of the environment, increasing sensitivity in quiet environments and decreasing sensitivity in loud environments. Cochlear sensitivity is regulated in part by olivocochlear efferent (OCE) neurons that transmit the signals from the brain to the cochlea. The OCE system uses multiple neurotransmitters and the different roles of each of these are not completely understood. CGRP is a peptide neurotransmitter used by the OCE system. To determine whether CGRP is involved in modulating sensitivity, we measured the Auditory Brainstem Response (ABR) amplitude, a physiological measure of hearing, in mice that were genetically altered to express higher levels of the CGRP receptor. This was done in collaboration with the Russo lab (Physiology). The results show that high levels of CGRP may sensitized receptors in the neurons that leads to no significant difference in ABR measures. In a second study we asked whether CGRP signaling is involved in modulating the sensitivity of the cochlea to loud, potentially damaging noise, focusing on noise damage to synapses in the cochlea. Preliminary data suggests that CGRP can sensitize afferent synapses to damage in vitro. We asked whether that is the case for noise exposure in vivo. Mice were exposed to noise at a level that causes moderate damage and injected with either CGRP or a CGRP antagonist. Hearing was subsequently measured by ABR to determine whether the treatments increased or decreased noise-induced hearing loss. "