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. Author manuscript; available in PMC: 2012 Apr 1.
Published in final edited form as: Pain. 2011 Feb 1;152(4):912–923. doi: 10.1016/j.pain.2011.01.016

Fig. 5.

Fig. 5

Persistent peripheral inflammation increases the proportion of Ca2+-permeable AMPARs in the extrasynaptic plasma membrane of tonic SG neurons. (A) A selective blocker of Ca2+-permeable AMPARs, IEM-1460 (40 μM), substantially inhibited AMPA-induced currents in tonic neurons of CFA-treated but not of saline-treated rats. Left, an overlay of AMPA-induced currents recorded in the absence (black traces) and presence (pre-incubation for 5 min; grey traces) of IEM-1460 24 h after saline or CFA. Right, IEM-1460 was bath applied during a steady-state phase of AMPA-induced current. Dotted lines represent exponential fitting of the currents; dotted arrow indicates the value of IEM-1460 inhibition. (B) A statistical summary of IEM-1460 inhibition of extrasynaptic AMPARs in tonic and transient SG neurons. *** p < 0.0001 versus the saline-treated group. (C) The top panel illustrates the protocol for reconstruction of the I-V relationship from ramp recordings. The bottom panel shows I-V curves obtained in tonic neurons at 24 h post-saline or post-CFA. Note that IEM-1460 reverses the rectification of AMPA-induced currents recorded from neurons of CFA-treated rats. (D, E) The scatter plot illustrates the spread in rectification index (RI = I+30mV/I−50mV) (D), and the bar graph shows the statistical summary for RI (E) in tonic neurons 24 h post-saline and post-CFA before (black) and after (grey) IEM-1460 application. *** p < 0.0001 versus the saline-treated group, ## p < 0.001 versus the CFA-treated group.