Fig. 3.

Efferent synaptic responses in rat type II hair cells (HCs) are mediated through α9-containing nicotinic acetylcholine receptors (nAChRs) and small-conductance potassium (SK) channels. A1: spontaneous excitatory postsynaptic currents (sEPSCs) were recorded in type II HCs at different holding potentials (V_h), as indicated at each trace. Biphasic responses at −60 mV and −70 mV are consistent with influx of cations (including calcium ions) through nAChRs followed by an outward current through calcium-activated K⁺ channels. A2: application of 1 mM ACh induced currents that showed a change from inward to outward currents at more positive V_h. A3: relative total charge transfer (normalized to charge transfer at −90 mV) at different V_h for synaptic currents (gray) and ACh-induced currents (black). B1 and B2: example recordings showing blockade of responses to application of 1 mM ACh by antagonists of α9-containing nAChRs [10 μM strychnine (Stry) or 600 nM α-RgIA]. Black, red, and blue traces show control (Ctrl), drug application, and post-wash conditions. B3: average effects of strychnine or α-RgIA (n = 3 type II HCs for each drug). C1 and C2: example recordings showing blockade of outward potassium currents in the presence of SK channel antagonist apamin (300 nM). Antagonist of large-conductance potassium (BK) channels [100 nM iberiotoxin (IBTX)] did not have any effect. C3: average effects of apamin (n = 3 type II HCs) and IBTX (n = 5 type II HCs). D1: 300 nM apamin blocked outward evoked synaptic currents (eEPSCs) at −50 mV. Three pulses at 100 Hz were used to trigger responses. Traces were averaged from 200 trials. D2: 300 nM apamin reversed the polarity of spontaneous synaptic currents. Traces were averaged from 15–20 events.