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Physiol. Genomics (October 10, 2001). doi:10.1152/physiolgenomics.00056.2001
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Articles in PresS, published online ahead of print October 10, 2001
Physiol Genomics, 10.1152/physiolgenomics.00056.2001
Submitted on July 11, 2001
Accepted on October 3, 2001

MASH-1/RET Pathway Involvement in Development of Brainstem Control of Respiratory Frequency in Newborn Mice

Stephane Dauger1, Fabien Guimiot2, Sylvain Renolleau2, Beatrice Levacher2, Bernadette Boda2, Christophe Mas2, Virginie Nepote2, Michel Simonneau2, Claude Gaultier3, and Jorge Gallego2*

1 E9935, INSERM, Paris, France; Pediatrie Reanimation, Hopital Robert Debre, Paris, France
2 E9935, INSERM, Paris, France
3 E9935, INSERM, Paris, France; Physiologie, Hopital Robert Debre, Paris, France

* To whom correspondence should be addressed. E-mail: gallego{at}idf.inserm.fr.

Respiratory abnormalities have been described in MASH-1 and c-RET mutant newborn mice. However, the neural mechanisms underlying these abnormalities have not been studied. We tested the hypothesis that the MASH-1 mutation may impair c-RET expression in brainstem neurones involved in the control of breathing. To do this, we analyzed brainstem c-RET expression and respiratory phenotype in MASH-1+/+ wild type, MASH-1+/- heterozygous, and MASH-1-/- knock-out newborn mice during the first two hours of life. In MASH-1-/- newborns, c-RET gene expression was absent in the noradrenergic nuclei (A2, A5, A6, A7) that contribute to modulate respiratory frequency and in scattered cells of the rostral ventrolateral medulla. The c-RET transcript levels measured by quantitative RT-PCR were lower in MASH-1-/- and MASH-1+/- than in MASH-1+/+ brainstems (P=0.001 and P=0.003, respectively). Breath durations were shorter in MASH-1-/- and MASH-1+/- than in MASH-1+/+ mice (P=0.022) and were weakly correlated with c-RET transcript levels (P=0.032). Taken together, these results provide evidence that MASH-1 is upstream of c-RET in noradrenergic brainstem neurons important for respiratory rhythm modulation.




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