Fig. 5.

D₂-like receptor activation increases rhythm stability and decreases rhythm frequency. A and B: spontaneous activity from single ventral root neurograms of the isolated spinal cord (A) were used to determine the IC₅₀ for D₂-mediated inhibition of motor output (B). The IC₅₀ for quinpirole was calculated as 12 μM by generating a response ratio between the root mean square of activity in a 10–20 min window after drug application compared with a 10-min baseline. Bath application of the D₂-like agonist quinpirole (20 μM) decreased the frequency (Cii and Ei) and increased stability (Cii and Eii) of a preexisting locomotor rhythm evoked by 5-HT and NMA (Ci). Similarly, bath application of the D₂-like antagonist sulpiride (20 μM) increased the frequency (Dii and Ei) but had no effect on stability (Dii and Eii) of a rhythm evoked by 5-HT, NMA, and dopamine (Di). Ei and Eii: bar graphs represent mean ± SE rhythm frequency (Ei) and power (Eii) normalized to baseline control rhythm conditions. Spectrograms depict cross-wavelet analysis of neurogram activity from left and right L₂ ventral roots over time, with the rhythm frequency on the y-axis and rhythm stability indicated by the power as the color bands. A more stable rhythm is displayed as warmer colors (C and D). Data are presented as mean ± SE normalized rhythm frequency (Ei) and power (Eii) over a 10-min window between 10 and 20 min after dopamine application and are normalized to a 10-min window of the control rhythm evoked by 5-HT and NMA. Significant differences from baseline control rhythm (repeated-measures ANOVA, Tukey post hoc) with *P < 0.05 and **P < 0.01.