Skip to main content
Figure 1 | Molecular Pain

Figure 1

From: Signal Transduction Mechanisms Underlying Group I mGluR-mediated Increase in Frequency and Amplitude of Spontaneous EPSCs in the Spinal Trigeminal Subnucleus Oralis of the Rat

Figure 1

Increase of sEPSC frequency and amplitude and change of Vt stimulation-evoked EPSC amplitude by bath application of DHPG in Vo. A diagram (A) demonstrates the recording site of the Vo area within the spinal trigeminal nucleus and the electrical stimulation site in the Vt. sEPSCs recorded at holding potential of -70 mV in the Vo area were blocked by 10 μM NBQX (B). Representative sEPSC traces at -70 mV, recorded from Vo neurons with Cs-based internal solution, before and during DHPG (10 μM, 5 min), the group I mGluR agonist, and after washout of the drug (Ca). Time-course graphs demonstrate DHPG-induced increases of sEPSC frequency (Cb) and amplitude (Cc) in Krebs's solution containing 5 μM BMI and 1 μM strychnine (n = 13). Each point with error bar represents mean ± SEM. Numbers on the graphs (Cb) indicate the corresponding time of the traces sampled. Representative EPSCs evoked by two pulses (interval, 50 ms) of Vt stimulation (Da). During DHPG, the amplitude of the first EPSC was slightly decreased, whereas that of the second EPSC increased (upper traces), resulting in an increase of paired pulse ratio (PPR, the second/the first EPSC). In traces (Da), the EPSC before DHPG was normalized to the amplitude of the first EPSCs during DHPG or after washout of DHPG (dotted line, normalized EPSCs). Histograms summarized the amplitude of the first EPSC (Db) and the PPR (Dc) before, during and after DHPG. The mean amplitude of EPSC was significantly increased after washout of DHPG, (Db, *P < 0.05, n = 5), whereas the mean PPR was significantly increased during DHPG (Dc, *P < 0.05, n = 8).

Back to article page