MafB deficiency causes defective respiratory rhythmogenesis and fatal central apnea at birth View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2003-10

AUTHORS

Bruno Blanchi, Louise M Kelly, Jean-Charles Viemari, Isabelle Lafon, Henri Burnet, Michelle Bévengut, Silke Tillmanns, Laurent Daniel, Thomas Graf, Gerard Hilaire, Michael H Sieweke

ABSTRACT

The genetic basis for the development of brainstem neurons that generate respiratory rhythm is unknown. Here we show that mice deficient for the transcription factor MafB die from central apnea at birth and are defective for respiratory rhythmogenesis in vitro. MafB is expressed in a subpopulation of neurons in the preBötzinger complex (preBötC), a putative principal site of rhythmogenesis. Brainstems from Mafb(-/-) mice are insensitive to preBötC electrolytic lesion or stimulation and modulation of rhythmogenesis by hypoxia or peptidergic input. Furthermore, in Mafb(-/-) mice the preBötC, but not major neuromodulatory groups, presents severe anatomical defects with loss of cellularity. Our results show an essential role of MafB in central respiratory control, possibly involving the specification of rhythmogenic preBötC neurons. More... »

PAGES

1091

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nn1129

DOI

http://dx.doi.org/10.1038/nn1129

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1027655421

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/14513037


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