ArticleNature communications2023
Phox2b-expressing neurons contribute to breathing problems in Kcnq2 loss- and gain-of-function encephalopathy models.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 7 citations in OpenAlex.
- μ-Opioid receptor signalling enhances Kir3 currents in glutamatergic preBötzinger complex neurons in mice.The Journal of physiology · 2026Article
- Effect of epileptogenesis on hypercapnic cardioventilatory response in kainic acid rats.Epilepsia · 2026Article
- GABAergic Inhibition from the Nucleus Tractus Solitarius to Ventrolateral Medulla Phox2b Neurons Modulates Central Respiratory Chemoreflex and Ventilatory Homeostasis.Neuroscience bulletin · 2026Article
- Mislocalization of KCNQ2 Channels as a Pathogenic Mechanism in KCNQ2 Developmental and Epileptic Encephalopathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- CRISPR/Cas9-mediatedFrontiers in physiology · 2026Article
- Oxytocinergic signalling in the respiratory parafacial region increases the activity of chemosensitive neurons and respiratory output.The Journal of physiology · 2025Article
- Retrotrapezoid nucleus chemoreception: mechanisms of function and contributions to disordered breathing in disease.Trends in neurosciences · 2025Review
- Sudden Unexpected Death in Epilepsy: Central Respiratory Chemoreception.International journal of molecular sciences · 2025Review
- Targeting Astrogliosis in the Retrotrapezoid Nucleus: A Novel Approach to Ameliorate Respiratory Dysfunction and Alzheimer's Pathology in Mice.Aging and disease · 2024Article
- Donepezil as a new therapeutic potential in KCNQ2- and KCNQ3-related autism.Frontiers in cellular neuroscience · 2024Article
- Linking Respiratory Challenges in KCNQ2 Encephalopathy to "Phox2b" Neurons in the Retrotrapezoid Nucleus.Epilepsy currentsArticle
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7 authors at 3 institutions in 1 country.
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Abstract
Loss- and gain-of-function variants in the gene encoding KCNQ2 channels are a common cause of developmental and epileptic encephalopathy, a condition characterized by seizures, developmental delays, breathing problems, and early mortality. To understand how KCNQ2 dysfunction impacts behavior in a mouse model, we focus on the control of breathing by neurons expressing the transcription factor Phox2b which includes respiratory neurons in the ventral parafacial region. We find Phox2b-expressing ventral parafacial neurons express Kcnq2 in the absence of other Kcnq isoforms, thus clarifying why disruption of Kcnq2 but not other channel isoforms results in breathing problems. We also find that Kcnq2 deletion or expression of a recurrent gain-of-function variant R201C in Phox2b-expressing neurons increases baseline breathing or decreases the central chemoreflex, respectively, in mice during the light/inactive state. These results uncover mechanisms underlying breathing abnormalities in KCNQ2 encephalopathy and highlight an unappreciated vulnerability of Phox2b-expressing ventral parafacial neurons to KCNQ2 pathogenic variants.
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