Figure 3

Minocycline inhibits CCL2-induced heat hyperalgesia and blocks CCL2-induced enhancement of glutamatergic transmission in substantia gelatinosa neurons. (A) Intrathecal administration of CCL2 (1 μg) decreased hind-paw withdrawal latency and caused heat hyperalgesia. Intrathecal co-injection of minocycline (100 μg) and CCL2 (1 μg) completely blocked the CCL2-induced reduction in the latency of hind-paw withdrawal and thermal hyperalgesia. Each bar shows mean ± standard error for 10 rats. *P < 0.01 compared to control rats. (B) One day after intrathecal administration of CCL2 (1 μg), the frequency of spontaneous mEPSCs was greatly increased a lamina II neuron. Intrathecal co-injection of CCL2 (1 μg) and minocycline (100 μg) inhibited the CCL2-induced increase in the frequency of mEPSCs in a lamina II neuron. V _H = -60 mV. (C) After intrathecal co-administration with minocycline, CCL2 did not significantly increase the frequency of mEPSCs in substantia gelatinosa neurons. Each bar shows mean ± standard error for 12 neurons from 6 rats. *P < 0.01 compared to control neurons. ^# P < 0.01 compared to CCL2-treated neurons. Con, control; mEPSC, miniature excitatory postsynaptic current.