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IDENTIFICATION OF NOVEL MEDULLARY NEURONS REGULATING NEONATAL BREATHING HOMEOSTASIS
Fanqi Mengand 1 co-author
Charite Universitatsmedizin Berlin
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-370
Presentation
Date TBA
Board: PS05-09AM-370
Event Information
Poster Board
PS05-09AM-370
Poster
View posterAbstract
Respiratory disorders are a leading cause of death and disability worldwide, yet the pathophysiological mechanisms underlying many of these conditions remain poorly understood. Congenital hypoventilation encompasses a diverse group of life-threatening disorders affecting newborns. One such condition, Congenital Central Hypoventilation Syndrome (CCHS), is characterized by pronounced hypoventilation, manifested as slow and shallow breathing, and central apnea during sleep. Patients with CCHS also exhibit impaired respiratory chemoreflexes, particularly in response to elevated blood CO₂ levels. Mutations in the genes encoding for the transcription factors PHOX2B and LBX1 are frequently observed in patients with congenital central hypoventilation, including those diagnosed with CCHS. Here, we show that developmental deficits in a medullary neuronal population co-expressing both transcription factors lead to hypoventilation, central apnea, and loss of CO₂ sensitivity in neonatal mice. Together, our findings identify a medullary neuron type with a critical role in the regulation of neonatal respiratory homeostasis.
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