The Journal of Neurophysiology Vol. 82 No. 6 December 1999, pp. 3307-3315
Copyright ©1999 by the American Physiological Society

Role of L-Type Ca²⁺ Channels in Transmitter Release From Mammalian Inner Hair Cells I. Gross Sound-Evoked Potentials

 ¹Department of Physiology, The Auditory Laboratory, The University of Western Australia, Nedlands, Western Australia 6907, Australia; and  ²Department of Otolaryngology, Guangdong Provincial People's Hospital, Guangzhou, People's Republic of China

Zhang, Si Yi, Donald Robertson, Graeme Yates, and Alan Everett. Role of L-Type Ca²⁺ Channels in Transmitter Release From Mammalian Inner Hair Cells I. Gross Sound-Evoked Potentials. J. Neurophysiol. 82: 3307-3315, 1999. Intracochlear perfusion and gross potential recording of sound-evoked neural and hair cell responses were used to study the site of action of the L-type Ca²⁺ channel blocker nimodipine in the guinea pig inner ear. In agreement with previous work nimodipine (1-10 µM) caused changes in both the compound auditory nerve action potential (CAP) and the DC component of the hair cell receptor potential (summating potential, or SP) in normal cochleae. For 20-kHz stimulation, the effect of nimodipine on the CAP threshold was markedly greater than the effect on the threshold of the negative SP. This latter result was consistent with a dominant action of nimodipine at the final output stage of cochlear transduction: either the release of transmitter from inner hair cells (IHCs) or the postsynaptic spike generation process. In animals in which the outer hair cells (OHCs) had been destroyed by prior administration of kanamycin, nimodipine still caused a large change in the 20-kHz CAP threshold, but even less change was observed in the negative SP threshold than in normal cochleae. When any neural contamination of the SP recording in kanamycin-treated animals was removed by prior intracochlear perfusion with TTX, nimodipine caused no significant change in SP threshold. Some features of the data also suggest a separate involvement of nimodipine-sensitive channels in OHC function. Perfusion of the cochlea with solutions containing Ni²⁺ (100 µM) caused no measurable change in either CAP or SP. These results are consistent with, but do not prove, the notion that L-type channels are directly involved in controlling transmitter release from the IHCs and that T-type Ca²⁺ channels are not involved at any stage of cochlear transduction.