@article {Gray14883, author = {Paul A. Gray and John A. Hayes and Guang Y. Ling and Isabel Llona and Srinivasan Tupal and Maria Cristina D. Picardo and Sarah E. Ross and Tsutomu Hirata and Joshua G. Corbin and Jaime Eugen{\'\i}n and Christopher A. Del Negro}, title = {Developmental Origin of PreB{\"o}tzinger Complex Respiratory Neurons}, volume = {30}, number = {44}, pages = {14883--14895}, year = {2010}, doi = {10.1523/JNEUROSCI.4031-10.2010}, publisher = {Society for Neuroscience}, abstract = {A subset of preB{\"o}tzinger Complex (preB{\"o}tC) neurokinin 1 receptor (NK1R) and somatostatin peptide (SST)-expressing neurons are necessary for breathing in adult rats, in vivo. Their developmental origins and relationship to other preB{\"o}tC glutamatergic neurons are unknown. Here we show, in mice, that the {\textquotedblleft}core{\textquotedblright} of preB{\"o}tC SST+/NK1R+/SST 2a receptor+ (SST2aR) neurons, are derived from Dbx1-expressing progenitors. We also show that Dbx1-derived neurons heterogeneously coexpress NK1R and SST2aR within and beyond the borders of preB{\"o}tC. More striking, we find that nearly all non-catecholaminergic glutamatergic neurons of the ventrolateral medulla (VLM) are also Dbx1 derived. PreB{\"o}tC SST+ neurons are born between E9.5 and E11.5 in the same proportion as non-SST-expressing neurons. Additionally, preB{\"o}tC Dbx1 neurons are respiratory modulated and show an early inspiratory phase of firing in rhythmically active slice preparations. Loss of Dbx1 eliminates all glutamatergic neurons from the respiratory VLM including preB{\"o}tC NK1R+/SST+ neurons. Dbx1 mutant mice do not express any spontaneous respiratory behaviors in vivo. Moreover, they do not generate rhythmic inspiratory activity in isolated en bloc preparations even after acidic or serotonergic stimulation. These data indicate that preB{\"o}tC core neurons represent a subset of a larger, more heterogeneous population of VLM Dbx1-derived neurons. These data indicate that Dbx1-derived neurons are essential for the expression and, we hypothesize, are responsible for the generation of respiratory behavior both in vitro and in vivo.}, issn = {0270-6474}, URL = {https://www.jneurosci.org/content/30/44/14883}, eprint = {https://www.jneurosci.org/content/30/44/14883.full.pdf}, journal = {Journal of Neuroscience} }