TrkC-CreERT2-mediated recombination supports evidence that TrkCTH DRG neurons contribute to cardiovascular homeostasis
Show moreAdd to Mendeleyhttps://doi.org/10.1016/j.celrep.2021.110260Get rights and contentopen access
HighlightsoThe TrkCCreERT2 BAC transgene does not fully reproduce the expression pattern of TrkC
oCre-mediated recombination is absent in nociceptors and sympathetic or vagal ganglia
oVasoconstriction is likely mediated by TrkC+/TH+ DRG neurons and not nociceptors
oStrategies targeting only TrkC+/TH+ DRG neurons are required to understand lethality
SummaryIn their Matters Arising article, McMullan et al. (2022) offer alternative explanations for the phenotypes we observed upon stimulation and ablation of TrkCCreERT2-positive neurons in mice. Their interpretations are focused on two aspects: first, whether the vasoconstriction we observed upon activation of TrkCCreERT2 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 TrkCCreERT2 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 TrkCCreERT2 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.
TrkC
dorsal root ganglia
pain
Recommended articlesCiting articles (0)
(C) 2021 The Author(s).
Recommended articlesNo articles found.
Citing articles
Belum ada Komentar untuk "TrkC-CreERT2-mediated recombination supports evidence that TrkCTH DRG neurons contribute to cardiovascular homeostasis"
Posting Komentar