Figure 6. The light-induced disruption of the locomotor-like rhythm is exacerbated in the presence of cholinergic antagonists.

(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 in the presence of 50 μM mecamylamine, 50 μM dhβE, and 5 μM atropine. The superimposed orange 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–E) Comparison between WT (black, brown), ChAT-Arch (green, orange) cords in the absence or presence of cholinergic antagonists. (B) Bar plot showing the average locomotor-like frequency in WT (n = 10) and ChAT-Arch (n = 6) cords under control conditions (no light) in the absence or presence of cholinergic antagonists (ANOVA, p<0.0001). (C–E) Bar plots showing the average change in the absolute phase (C), 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 (Start Light, circles) for WT (black, brown), ChAT-Arch (green, orange) cords in the absence or presence of cholinergic antagonists. Using a two-way ANOVA we calculated the statistical differences between the three groups of animals (genetic Identity, shown above the bars) and the differences between light on and light off (light status, shown below the bars). The results of the ANOVA for the changes in the variables were: absolute phase (Light status: F (3,112) p<0.0001, Genetic identity/Drug treatment: F(3,112) p<0.0001, Interaction F(9,112) p=0.0017), frequency (Light status: F (3,112) p<0.0001, Genetic identity/Drug treatment: F(3,112) p=0.3073, Interaction F(9,112) p<0.0001), and motoneuron firing (Light status: F (3,112) p<0.0001, Genetic identity/Drug treatment: F(3,112) p<0.0001, Interaction F(9,112) p<0.0001). *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

DOI: http://dx.doi.org/10.7554/eLife.26622.022

Figure 6—figure supplement 1. Effect of green light during drug-induced locomotor-like in wild type cords in the presence of cholinergic blockers.

(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 50 μM mecamylamine, 50 μM dhβE, and 5 μM atropine (n = 10). The superimposed brown 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 line represents one standard deviation of the mean. Except for an increase in the firing of the ipsilateral/flexor extensor roots and a small phase change at light onset, the light (green rectangles) does not result in systematic changes in the other variables.

DOI: http://dx.doi.org/10.7554/eLife.26622.027