Figure 2: Cholesterol depletion reduces the amplitude of RA currents in sensory neurons.

(a) Representative traces of RA-mechanosensitive currents recorded in control or MβCD-treated neurons. Quantitative comparison of the peak amplitude (b), latency and inactivation time constant (c) of the RA currents (unpaired t-test, peak amplitude, P<0.01; latency, P>0.05; inactivation time constant τ, P>0.05). See also Supplementary Table 1. (d) Representative traces of RA currents activated by increasing membrane displacement (from 128 to 512 nm). (e) Relationship between displacement and peak current. Data were fitted with Boltzmann distributions (control, R²=0.82; MβCD, R²=0.79). See also Supplementary Table 2 and Supplementary Fig. 1. (f) Representative traces of RA currents activated by increasing probe velocity (from 341 to 4,654 μm s⁻¹). (g) Stimulus–response curve of RA currents evoked by increasing probe velocity (two-way ANOVA, P<0.01). See also Supplementary Fig. 1. (h) Example traces of RA currents evoked by 0.2-Hz 512-nm mechanical stimulus trains. (i) No decay in the magnitude of RA currents evoked by a 0.2-Hz mechanical stimulus train in either control or MβCD-treated neurons (time effect: one-way ANOVA, control P>0.05, MβCD P>0.05; control versus MβCD, two-way ANOVA, P>0.05). The number of neurons recorded is indicated in parentheses in each panel. **P<0.01; Error bars indicate s.e.m.