Figure 1

Intrathecal administration of CCL2 induces heat hyperalgesia and increases the magnitude of evoked glutamatergic EPSCs of substantia gelatinosa neurons. (A) CCL2 (1 μg) was intrathecally injected into 2-month-old rats. One day after the injection, the hot plate assay was used to measure hind-paw withdrawal latency. As a control, the vehicle was intrathecally injected into rats. Compared to wild-type (WT) rats and rats intrathecally administrated with the vehicle, the latency of hind-paw withdrawal caused by the heat stimulus was significantly reduced in the rats intrathecally injected with CCL2. Note that co-administration of CCR2 antagonist BMS CCR2 22 with CCL2 completely blocked CCL2-induced thermal hyperalgesia. Each bar shows the mean ± standard error for 12 or 20 rats. *P < 0.01 compared to wild-type rats. (B) One day after intrathecally injecting the vehicle or CCL2 (1 μg) into the rats, glutamatergic EPSCs were evoked by a stimulating electrode placed at the dorsal root entry zone and recorded from an outer lamina II neuron in a spinal cord slice prepared from a vehicle- or CCL2-treated rat. Compared to representative EPSCs evoked by various magnitudes of stimulation currents for control rats, the amplitude of representative EPSCs was significantly higher for lamina II neurons of CCL2-treated rats. (C) Slope of input–output curve for evoked EPSCs was significantly increased in substantia gelatinosa neurons of CCL2-injected rats. Each point represents the mean ± standard error for 13 to 15 neurons from seven rats. Holding potential (V _H ) was -60 mV. *P < 0.01 compared to control neurons.