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. 2017 Jul 3;6:e26622. doi: 10.7554/eLife.26622

Figure 9. The light-induced disruption of the locomotor-like rhythm is attenuated in the presence of the AMPA-receptor antagonist NBQX.

(A) Ventral root recordings (Right L2, and Left L2 and L5) showing the effect of green light on the locomotor-like rhythm evoked by 5 μM NMDA and 10 μM 5-HT in the presence of 10 μM NBQX. The superimposed light purple traces are the slow potentials obtained by low pass filtering the raw signal. The green bar indicates the duration of the light. (B) Bar plot showing the average locomotor-like frequency in WT (n = 6) and ChAT-Arch (n = 7) cords under control conditions (no light) in the absence or presence of NBQX. For both WT and ChAT-Arch animals the frequency of the rhythm is significantly slower in the presence of NBQX. ANOVA, p<0.0001 (C–E) Bar plots showing the average change in the absolute phase (C) and frequency (D) of the bilateral flexors for the 10 s just before and just after the light is turned on (Start Light, circles) and the 10 s just before and just after the light is turned off (After Light, squares). (E) Bar plot showing the averaged integrated neurogram (Change in MN firing) of the ipsilateral flexor root for the 10 s just before and just after the light is turned on for WT (black, dark purple), ChAT-Arch (green, light purple) cords in the absence or presence of NBQX. Using a two-way ANOVA, we calculated the statistical differences between the different groups of animals (genetic identity, shown above the bars) and the differences between light on and light off (light status; shown below the bars). (B–C–D–E) Comparison between WT (black, dark purple), ChAT-Arch (green, light purple) cords in the absence or presence of NBQX. The results of the ANOVA for the changes in the phase were (Light status: F (3,88) p=0.2436, genetic identity/Drug treatment: F(3,88) p<0.0001, interaction F(9,88) p=0.3893), for the frequency were (Light status: F (3,88) p=0.0630, Genetic identity/Drug treatment: F(3,88) p=0.1335, interaction F(9,88) p<0.0001) and for the motoneuron firing were (Light status: F (3,88) p<0.0001, Genetic identity/Drug treatment: F(3,88) p=0.0001, interaction F(9,88) p<0.0001). *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

DOI: http://dx.doi.org/10.7554/eLife.26622.037

Figure 9—source data 1. Source data for Bar plots in Figure 9B.
DOI: 10.7554/eLife.26622.038
Figure 9—source data 2. Source data for Bar plots in Figure 9C.
DOI: 10.7554/eLife.26622.039
Figure 9—source data 3. Source data for Bar plots in Figure 9D.
DOI: 10.7554/eLife.26622.040
Figure 9—source data 4. Source data for Bar plots in Figure 9E.
DOI: 10.7554/eLife.26622.041

Figure 9.

Figure 9—figure supplement 1. Effect of green light on drug-induced locomotor-like activity in wild type cords in the presence of NBQX.

Figure 9—figure supplement 1.

(A) Ventral root recordings (Right L2, and Left L2 and L5) showing the effect of light on the locomotor-like rhythm evoked by 5 μM NMDA and 10 μM 5-HT in the presence of 10 μM NBQX in wild type cords (n = 6). The superimposed dark purple traces are the slow potentials obtained by low pass filtering the raw signal. The green bar indicates the duration of the light (60 s). (B–C) Time series of the change in absolute phase (B) and frequency (C) averaged for all experiments for the bilateral flexor (B1–C1) and ipsilateral flexor-extensor roots (B2–C2). (D) Averaged integrated signals (Change in MN Firing) for the ipsilateral flexor (D1) and extensor (D2) ventral roots. The grey dotted lines represent one standard deviation of the mean. The most prominent effect of the light (green rectangles) is a transient increase in frequency at light onset.