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. 2020 Feb 13;11:869. doi: 10.1038/s41467-019-14154-6

Fig. 7. CLP257 protects from dynamic collapse in Cl− gradient under a barrage of inhibitory inputs.

Fig. 7

a Three representative traces of repetitive inhibitory stimulation (20 Hz, 25 stimulations) at 0 mV in PNI, with ACSF (gray trace), with L838,417 (2 µM, black trace) applied in the bath or with L838,417 and CLP257 (100 µM, red trace) of transversal spinal cord sections. The depression of eIPSCs at 0 mV was amplified by L838,417 in PNI due to Cl− accumulation and can be reversed by CLP257. Stimulus artefacts have been canceled. b Representative traces showing the increase in amplitudes and decay times with L838,417 with or without CLP257 vs. ACSF on averaged eIPSCs evoked at 1 Hz. Inset shows the sames traces scaled to peak for kinetics comparison. c Averaged eIPSC amplitude depression at 0 mV during the repetitive inhibitory stimulation protocol in two pharmacological conditions: L838,417 (2 μm) and L838,417 (2 μm) + steady-state of CLP257 (5 μM) incubations (one phase decay fits; n = 5 neurons per condition). d same stimulations and recording conditions with at least 15 min of pre-incubation of the following conditions: ACSF, L838,417 (2 μm), L838,417 (2 μm) + CLP257 (100 μM) (one phase decay fits; n = 3 to 4 neurons per condition). e same as c with a holding potential of −90 mV instead of 0 mV. f same as d with a holding potential of -90 mV instead of 0 mV. eIPSC amplitude were normalized to the average of the first three eIPSCs generated by the 20 Hz stimulation. (*P < 0.05). Source data is available as a Source Data file.