Presynaptic voltage-gated calcium channels in the auditory brainstem

Abstract

Sound information encoding within the initial synapses in the auditory brainstem requires reliable and precise synaptic transmission in response to rapid and large fluctuations in action potential (AP) firing rates. The magnitude and location of Ca²⁺ entry through voltage-gated Ca²⁺ channels (Ca_V) in the presynaptic terminal are key determinants in triggering AP-mediated release. In the mammalian central nervous system (CNS), the Ca_V2.1 subtype is the critical subtype for CNS function, since it is the most efficient Ca_V2 subtype in triggering AP-mediated synaptic vesicle (SV) release. Auditory brainstem synapses utilize Ca_V2.1 to sustain fast and repetitive SV release to encode sound information. Therefore, understanding the presynaptic mechanisms that control Ca_V2.1 localization, organization and biophysical properties are integral to understanding auditory processing. Here, we review our current knowledge about the control of presynaptic Ca_V2 abundance and organization in the auditory brainstem and impact on the regulation of auditory processing.

Keywords: Auditory brainstem; Auditory information processing; Hearing; Presynaptic mechanisms; Synaptic transmission; Voltage-gated calcium channels.