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Voltage-gated L-type Ca 2+  channels (L-VGCCs) like Ca V 1.2 are assumed to play a crucial role for controlling release of trophic peptides including brain-derived neurotrophic factor (BDNF). In the inner ear of the adult mouse, besides the well-described L-VGCC Ca V 1.3, Ca V 1.2 is also expressed. Due to lethality of constitutive Ca V 1.2 knock-out mice, the function of this ion channel as well as its putative relationship to BDNF in the auditory system is entirely elusive. We recently described that BDNF plays a differential role for inner hair cell (IHC) vesicles release in normal and traumatized condition. To elucidate a presumptive role of Ca V 1.2 during this process, two tissue-specific conditional mouse lines were generated. To distinguish the impact of Ca V 1.2 on the cochlea from that on feedback loops from higher auditory centers Ca V 1.2 was deleted, in one mouse line, under the Pax2 promoter (Ca V 1.2 Pax2 ) leading to a deletion in the spiral ganglion neurons, dorsal cochlear nucleus, and inferior colliculus. In the second mouse line, the Egr2 promoter was used for deleting Ca V 1.2 (Ca V 1.2 Egr2 ) in auditory brainstem nuclei. In both mouse lines, normal hearing threshold and equal number of IHC release sites were observed. We found a slight reduction of auditory brainstem response wave I amplitudes in the Ca V 1.2 Pax2  mice, but not in the Ca V 1.2 Egr2  mice. After noise exposure, Ca V 1.2 Pax2  mice had less-pronounced hearing loss that correlated with maintenance of ribbons in IHCs and less reduced activity in auditory nerve fibers, as well as in higher brain centers at supra-threshold sound stimulation. As reduced cochlear BDNF mRNA levels were found in Ca V 1.2 Pax2  mice, we suggest that a Ca V 1.2-dependent step may participate in triggering part of the beneficial and deteriorating effects of cochlear BDNF in intact systems and during noise exposure through a pathway that is independent of Ca V 1.2 function in efferent circuits.

frontiers in molecular neuroscience

L-type CaV1.2 deletion in the cochlea but not in the brainstem reduces noise vulnerability: implication for CaV1.2-mediated control of cochlear BDNF expression