Skip to main content
. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: Pain. 2015 Sep;156(9):1737–1746. doi: 10.1097/j.pain.0000000000000208

Figure 4.

Figure 4

CXCL10 increased neuronal membrane excitability after CHS. In each panel, neurons were tested that exhibited DiI labeling transported from SADBE challenged skin. A, Typical current clamp recordings of CXCL10-induced membrane potential depolarization and action potential discharges. Black bars above the traces indicates the duration of CXCL10 (50 nM; 2 min) application. B–C, Mean resting membrane potential (RMP) and mean input resistance (Rin) before (control) and during application of CXCL10. CXCL10 significantly depolarized the RMP and reduced the Rin. *p < 0.05 versus control, paired t tests. D, Representative current clamp recordings of CXCL10 application in presence of AMG487 (10 μM). E–F, Pretreatment with AMG487 significantly reduced the mean magnitude of CXCL10-induced membrane depolarization (paired t test) and decreased the incidence (percentage) of neurons exhibiting action potentials (Fisher’s Exact test). The number of cells responding and/or tested are in parentheses. *p < 0.05 versus control.