Fig. 6.
Direct application of N-acylphenolamine (AM404), but not acetaminophen, to the spinal cord of inflammatory pain model rats increases the frequency of miniature excitatory postsynaptic currents (mEPSCs) sensitive to presynaptic transient receptor potential vanilloid 1 on substantia gelatinosa neurons. (A) Direct administration of acetaminophen (30 μM, 2 min) to the spinal cord of inflammatory pain model rats did not change the amplitude or frequency of mEPSCs in substantia gelatinosa neurons (n = 7). The top horizontal scale bar represents 30 s, and the top vertical bar represents 10 pA. The bottom horizontal scale bar represents 500 ms, and the bottom vertical bar represents 10 pA. (B) Direct administration of AM404 (30 μM, 2 min) to the spinal cord did not change the mean mEPSC amplitude and had no effect on the cumulative distribution of mEPSC amplitudes. In contrast, AM404 significantly increased the mean mEPSC frequency and induced a significant leftward shift in the cumulative interevent interval distribution of mEPSCs (n = 7; *P < 0.05, **P < 0.01, paired Student’s t test). The top horizontal scale bar represents 30 s, and the top vertical bar represents 10 pA. The bottom horizontal scale bar represents 500 ms, and the bottom vertical bar represents 10 pA. (C) In the presence of the transient receptor potential vanilloid 1 receptor antagonist, capsazepine (CPZ; 10 μM), the AM404-induced increase in mEPSC frequency was not observed (n = 7). Miniature EPSCs were measured using in vitro whole cell patch-clamp recordings. The horizontal scale bar represents 30 s, and the vertical bar represents 10 pA. The data are given as means ± SDs. TTX = tetrodotoxin.