Extended Data Figure 9. Controls for optogenetic activation of terminals of cVLM^TH-neurons in the LC.

Related to Figure 7. A. Experimental paradigm used to examine the influence of spinal cord NA on cVLM^TH neuron induced antinociceptive effects. B. Optogenetic activation of cVLM^TH neuron fiber terminals in the LC induced increased withdrawal latencies in Hargreaves test which were significantly attenuated by intrathecal administration of yohimbine, n=8 mice, p=0.0001 for L and p=0.017 for R hind-paws respectivelytwo-sided paired t-test, data represent means ± SEM. C. Serotonin 5-hydroytryptamine type 3 (5-HT3) receptor antagonist ondansetron (suggested to be responsible, in part, for descending facilitation of pain from the RVM) had no effect on CNO-induced pronociception elicited by chemogenetic inhibition of cVLM^TH neuron, n=7 mice, p=0.49 for L and p=0.17 for R hind-paws. D. Similarly, 5-hydroytryptamine type 7 (5-HT7) receptor agonist, AS19 (thought to be responsible, in part, for the descending inhibition of pain from the RVM) also did not affect CNO-induced pronociception, n=7 mice, p=0.59 for L and p=0.0.20 for R hind-paws,two-sided paired t-test, data are presented as mean ± SEM.