L-type calcium channel modulation reveals the relationship between neuronal synchrony and hyperactivity in the inferior colliculus following noise-induced hearing loss

Abstract

Abstract Previous studies have established the protective effects of calcium channel inhibition on the peripheral auditory system in response to noise exposure. While these studies implicate L-type calcium channels (LTCCs) in noise-generated dysfunction in the auditory periphery, contributions of LTCCs to noise-induced central dysfunction remains unclear. To begin to elucidate the roles of LTCCs in hearing, peripheral and central auditory function were assessed longitudinally after LTCC inhibition. Neuronal synchrony and activity were assessed by analyzing wave I (peripheral) and wave V (central) auditory brainstem responses (ABRs). Just prior to a noise exposure resulting in a temporary shift in hearing thresholds, rats were administered verapamil (LTCC blocker) or saline. Verapamil administration prevented the noise-induced decrease in ABR wave I and V amplitudes. Interestingly, when non-noise exposed animals were administered verapamil, wave V amplitude decreased, suggesting that LTCCs are critical for neuronal synchrony in the inferior colliculus. The inferior colliculus mediates gap inhibition of the acoustic startle reflex (giASR). Following noise exposure, giASR was enhanced, but the enhancement was not prevented by LTCC antagonism. These results suggest that while LTCCs are necessary for auditory-related synchronous activity, these channels do not directly contribute to noise-induced hyperactivity in the inferior colliculus.