About this Research Topic
Central respiratory chemoreceptors are key players for adjusting breathing to physiological demands and for systemic CO 2 and H + homeostasis. Neurons and/or astrocytes within specific brain regions sense elevated H + and/or CO 2 , and activate the respiratory neural network leading to increased ventilation. Failure in central chemoreception is a known feature of life-threatening
human conditions such as Congenital Central Hypoventilation Syndrome (CCHS), Sudden Infant Death Syndrome (SIDS), Sudden Unexpected Death in Epilepsy (SUDEP) and Rett
Syndrome (RS). The mechanisms involved in these pathologies are poorly understood.
The goals of this Research Topic are to expand knowledge about the main role of central chemoreceptors in breathing regulation, the common and different mechanisms found in central chemoreception along the vertebrate lineage, and how perinatal risk factors can affect central chemoreception in postnatal life. The emphasis of this collection of papers is on new evidence that points to different mechanisms for respiratory chemoreception than has been favored in the field in recent years, and indicates that much more work needs to be done to understand this vital function in health and disease.
We are interested in original data articles, reviews or hypotheses manuscripts addressing the following specific themes:
1) Central respiratory chemoreception as a characteristic function. Once believed to involve only a limited number of specialized neurons in specific regions, more varied hypotheses have recently been proposed. The Research Topic will include studies indicating that central chemoreception involves a variety of disparate mechanisms along the vertebrate lineage including work that indicates that glia play an important role in facilitating the respiratory response to hypercapnia;
2) Central chemoreception as an emergent property arising from the interaction of well recognized chemosensory areas. For example, recent work suggests that serotonergic raphe neurons are essential for expression of chemosensory responses of neurons in the retrotrapezoid nucleus (RTN), a notion not consistent with mainstream dogma. Such interactions may lead to a greater response than would occur based on mechanisms present in a single set of neurons acting alone;
3) Central respiratory chemoreception as a vulnerable property affected by perinatal risk factors,
which will be expressed in respiratory dysfunctions during postnatal life. We expect to receive studies based on animal models giving insights to understand the mechanisms through which
perinatal challenges increase chemosensory vulnerability that leads to postnatal respiratory failure in human pathologies.
Topic Editor Dr. George Richerson received a grant in 2021 from Neurava, which designs wearable devices to monitor epilepsy and seizures. The other Topic Editor declares no competing interests.
Keywords: Hypercapnia, Central chemoreceptors, Central Congenital Hypoventilation Syndrome (CCHS), Sudden Infant Death Syndrome (SIDS), Rett Syndrome (RS), Raphe nuclei, Retrotrapezoid nuclei, Brainstem, Prenatal nicotine exposure, chemosensitivity
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