Skip to main content
. Author manuscript; available in PMC: 2018 Sep 19.
Published in final edited form as: Science. 2016 Nov 10;354(6316):1144–1148. doi: 10.1126/science.aah5715

Fig. 3. HFS-induced LTP in vivo depends on spinal glial cells and d-serine signaling.

Fig. 3

Area of C-fiber–evoked field potentials was normalized to baseline values before conditioning HFS and plotted against time (min). Data are expressed as mean ± 1 SEM. Horizontal bars indicate drug application. (A) Mean time course of LTP of C-fiber–evoked field potentials. HFS at time point 0 min (arrow) induced LTP in all animals tested (n = 49, P < 0.001). One hour after HFS, the superfusate was collected from the lumbar spinal cord dorsum and transferred to animals shown in Fig. 4. (B) Spinal superfusion with the glial inhibitor fluoroacetate (10 μM) fully blocked HFS-induced potentiation in all animals tested (n = 15, P = 0.085). (C) HFS-induced LTP was fully prevented by spinal superfusion with DAAO (1 U·ml−1; n = 6, P = 0.365). Insets show original traces of field potentials recorded at indicated time points. Calibration bars indicate 0.2 mV and 50 ms. RM ANOVA on ranks was performed to determine statistical significance in (A). In all other experiments, data were analyzed by using RM ANOVA.