Figure 3.

Phase-locking and the Ca²⁺ current. (A) Idealized traces showing a sinusoidal receptor potential (V_MET; black line) and resulting Ca²⁺ current (I_Ca; red line) in response to a 400 Hz sound wave with a low (upper panel) and high (lower panel) intensity. The horizontal dashed line indicates the adult mouse IHC resting membrane potential (V_rest = −60 mV; Johnson et al., 2011). Asterisks indicate peak of I_Ca (red) and of V_MET depolarization (black). The resulting increase in intracellular [Ca²⁺] elicits phase-locked M-EPSCs (green trace; M-EPSC re-drawn from Glowatzki and Fuchs, 2002) which are encoded in action potentials at the primary auditory afferents (blue trace). One EPSC can trigger only one spike (Rutherford et al., 2012), while no vesicles would be released during interspike intervals (i.e., spike discharge would reflects vesicle release probability; Moezzi et al., 2014). As a result of the increased Ca²⁺ channel P_o with IHC depolarization, louder sounds (bottom panel) elicit more action potentials (less failures) with the same timing (phase-locking), as indicated by the vertical dashed lines. Note that, as shown in the bullfrog auditory papilla (Figure 5 in Li et al., 2014), I_Ca phase-lags V_MET, while M-EPSCs only occur in the V_MET repolarizing phase. Action potentials further lag V_MET due to the time required by electrotonic currents to depolarize the encoder region up to the spiking voltage threshold (~0. 5 ms; Rutherford et al., 2012). (B) Idealized elementary and macroscopic Ca²⁺ currents elicited by a voltage step from the resting membrane potential of −70 mV to −50 mV (top) or −20 mV (bottom). Activation kinetics of the macroscopic current re-drawn from Johnson and Marcotti (2008), deactivation kinetics re-drawn from Zampini et al. (2014). Increasing IHC depolarization reduces the latency and the time-to-peak of i_Ca and I_Ca, while it decreases or increases the amplitude of i_Ca or I_Ca, respectively.