Probing Functional Properties of Nociceptive Axons Using a Microfluidic Culture System
Figure 6
Using patch clamp electrophysiology to study impact of sodium channel blockers on axonal function.
(A) The top trace shows control somal responses to electrical stimulation of axons (1 mA, 2 ms duration stimuli, applied in 5 s, 5 Hz trains, with 20 s inter-train intervals). Addition of 0.5 μM TTX to the middle axonal channel completely inhibited somal APs, however increasing stimulus intensity to 2 mA restored the somal response. Subsequent application of lidocaine to the middle channel in this cell abolished responses which could not be restored with higher stimulus intensities. Washout reversed the inhibitory effects of lidocaine. Application of lidocaine to the far stimulation channel (bottom trace) had no effect on the somal response. (B) The top trace shows control responses to electrical stimulation of axons (5 mA, 2 ms duration stimuli, applied in 10 s, 2.2 Hz trains, with 10 s inter-train intervals). The addition of the Nav1.8 blocker A-803467 (1 μM) to the middle axonal channel in this cell increased the somal spike failure rate. Washout reversed the effects of A-803467 and the lower trace shows complete abolition of somal responses following axonal application of lidocaine (middle channel).