Journal
JOURNAL OF NEUROSCIENCE
Volume 30, Issue 28, Pages 9465-9476Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1765-10.2010
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- Centre Nationale de la Recherche Scientifique
- French Muscular Dystrophy Association (AFM)
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Neonatal breathing in mammals involves multiple neuronal circuits, but its genetic basis remains unclear. Mice deficient for the zinc finger protein Teashirt 3 (TSHZ3) fail to breathe and die at birth. Tshz3 is expressed in multiple areas of the brainstem involved in respiration, including the pre-Botzinger complex (preBotC), the embryonic parafacial respiratory group (e-pF), and cranial motoneurons that control the upper airways. Tshz3 inactivation led to pronounced cell death of motoneurons in the nucleus ambiguus and induced strong alterations of rhythmogenesis in the e-pF oscillator. In contrast, the preBotC oscillator appeared to be unaffected. These deficits result in impaired upper airway function, abnormal central respiratory rhythm generation, and altered responses to pH changes. Thus, a single gene, Tshz3, controls the development of diverse components of the circuitry required for breathing.
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