TrkC-CreERT2-mediated recombination supports evidence that TrkC(+)/TH+ DRG neurons contribute to cardiovascular homeostasis

In their Matters Arising article, McMullan et al. (2022) offer alternative explanations for the phenotypes we observed upon stimulation and ablation of TrkC(CreERT2)-positive neurons in mice. Their interpretations are focused on two aspects: first, whether the vasoconstriction we observed upon activation of TrkC(CreERT2) neurons is really mediated by TrkC/TH-positive neurons, or whether it might stem from stimulation of somatic nociceptors that also express TrkC; and second, whether the lethality observed after ablation of TrkC(CreERT2) neurons might be a result of ablation of vagal afferents and not TrkC/TH neurons located in the spinal ganglia. Central to both of these concerns is the expression and recombination efficiency of the TrkC(CreERT2) transgene in these other cell types. This Matters Arising Response paper addresses the McMullan et al. (2022) Matters Arising paper, published concurrently in Cell Reports.