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Cochlear frequency selectivity in lower vertebrates arises in part from electrical tuning intrinsic to the sensory hair cells. The resonant frequency is determined largely by the gating kinetics of calcium-activated potassium (BK) channels encoded by the slo gene. Alternative splicing of slo from chick cochlea generated kinetically distinct BK channels. Combination with accessory beta subunits slowed the gating kinetics of alpha splice variants but preserved relative differences between them. In situ hybridization showed that the beta subunit is preferentially expressed by low-frequency (apical) hair cells in the avian cochlea. Interaction of beta with alpha splice variants could provide the kinetic range needed for electrical tuning of cochlear hair cells.

Cochlear hair cells are inhibited by cholinergic efferent neurons. The acetylcholine (ACh) receptor of the hair cell is a ligand-gated cation channel through which calcium enters to activate potassium channels and hyperpolarize the cell. It has been proposed that calciuminduced calcium release (CICR) from a near-membrane postsynaptic store supplements this process. Here, we demonstrate expression of type I ryanodine receptors in outer hair cells in the apical turn of the rat cochlea. Consistent with this finding, ryanodine and other store-active compounds alter the amplitude of transient currents produced by synaptic release of ACh, as well as the response of the hair cell to exogenous ACh. Like the sarcoplasmic reticulum of muscle, the "synaptoplasmic" cistern of the hair cell efficiently couples synaptic input to CICR.

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Type II cochlear afferents receive glutamatergic synaptic excitation from outer hair cells (OHCs) in the rat cochlea. However, it remains uncertain whether this connection is capable of providing auditory information to the brain. The functional efficacy of this connection depends in part on the number of presynaptic OHCs, their probability of transmitter release, and the effective electrical distance for spatial summation in the Type II fiber. The present work addresses these questions using whole-cell recordings from the spiral process of type II afferents that run below OHCs in the apical turn of young (5–9 days postnatal) rat cochlea. A ‘high potassium puffer’ was used to elicit calcium action potentials from individual OHCs and thereby show that the average probability of transmitter release was 0.26 (range 0.02 to 0.73). Electron microscopy showed relatively few vesicles tethered to ribbons in equivalent OHCs. A ‘receptive field’ map for individual type II fibers was constructed by successively puffing onto OHCs along the cochlear spiral, up to 180 µm from the recording pipette. These revealed a conservative estimate of 7 presynaptic OHCs per type II fiber (range 1–11). EPSCs evoked from presynaptic OHCs separated by more than 100 µm did not differ in amplitude or waveform, implying that the type II fiber’s length constant exceeded the length of the synaptic input zone. Taken together these data suggest that type II fibers could communicate centrally by maximal activation of their entire pool of presynaptic OHCs.

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Native Ca V 1.3 channels within cochlear hair cells exhibit a surprising lack of Ca 2ϩ -dependent inactivation (CDI), given that heterologously expressed Ca V 1.3 channels show marked CDI. To determine whether alternative splicing at the C terminus of the Ca V 1.3 gene may produce a hair cell splice variant with weak CDI, we transcript-scanned mRNA obtained from rat cochlea. We found that the alternate use of exon 41 acceptor sites generated a splice variant that lost the calmodulin-binding IQ motif of the C terminus. These Ca V 1.3 IQ⌬ ("IQ deleted") channels exhibited a lack of CDI, which was independent of the type of coexpressed ␤-subunits. Ca V 1.3 IQ⌬ channel immunoreactivity was preferentially localized to cochlear outer hair cells (OHCs), whereas that of Ca V 1.3 IQfull channels (IQ-possessing) labeled inner hair cells (IHCs). The preferential expression of Ca V 1.3 IQ⌬ within OHCs suggests that these channels may play a role in processes such as electromotility or activity-dependent gene transcription rather than neurotransmitter release, which is performed predominantly by IHCs in the cochlea.

Ribbon synapses formed between inner hair cells (IHCs