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

被引：140
作者：
Blanchi, B
Kelly, LM
Viemari, JC
Lafon, I
Burnet, H
Bévengut, M
Tillmanns, S
Daniel, L
Graf, T
Hilaire, G
Sieweke, MH
机构：
[1] Univ Mediterrane, INSERM, CNRS, Ctr Immunol Marseille Luminy, F-13288 Marseille 09, France
[2] CNRS, Grp Etud Reseaux Moteurs, F-13009 Marseille, France
[3] Fac Med Timone, IBDM, Lab Pathol Nerveuse & Musculaire, F-13005 Marseille, France
[4] Yeshiva Univ Albert Einstein Coll Med, Bronx, NY 10461 USA
来源：
NATURE NEUROSCIENCE | 2003年 / 6卷 / 10期
关键词：
D O I：
10.1038/nn1129
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
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 preBotzinger complex (preBotC), a putative principal site of rhythmogenesis. Brainstems from Mafb(-/-) mice are insensitive to preBotC electrolytic lesion or stimulation and modulation of rhythmogenesis by hypoxia or peptidergic input. Furthermore, in Mafb(-/-) mice the preBotC, 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 preBotC neurons.
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收藏
页码：1091 / 1099
页数：9
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