The frequency of spontaneous AD is reduced by silencing spinal glutamatergic interneurons. Radiotelemetry devices were implanted 3 d before mice received a complete T3 SCI. Heart rate and blood pressure were recorded from −3 to 30 d post-SCI. To silence Gi DREADD-transduced VGluT2 interneurons, mice were injected with CNO (1 mg/kg, i.p.) 2–3×/d starting at 14 dpi. Control mice were injected with saline. A, Time post-injury versus the number of daily AD events. Data pooled from two replicate experiments and analyzed using a mixed-effect model to compare slopes; n = 7–8 mice/group in each replicate study (total saline, n = 15; CNO, n = 16); **p < 0.01 comparing slopes; values are the mean ± SEM. B, The average number of daily spontaneous AD events grouped by week after T3 SCI. Mixed-effects model with Bonferroni post hoc test; n = 7–8 mice/group in each replicate study (total saline, n = 15; CNO, n = 16); ap < 0.01 comparing groups at matched time points; values are the mean ± SEM. C, The maximum number of daily AD events recorded between 14 and 30 dpi is reduced by silencing VGluT2+ interneurons with CNO. Mann–Whitney U test comparing groups; n = 15–16 mice/group; bp < 0.0001; values are the mean ± SEM.