ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Expression of multiple P2X receptors by glossopharyngeal neurons projecting to rat carotid body O2-chemoreceptors: role in nitric oxide-mediated efferent inhibition.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 54 citations in OpenAlex.
- Type II Cells in the Human Carotid Body Display P2X7 Receptor and Pannexin-1 Immunoreactivity.Biomolecules · 2025Article
- Translating physiology of the arterial chemoreflex into novel therapeutic interventions targeting carotid bodies in cardiometabolic disorders.The Journal of physiology · 2025Review
- Intra-carotid body inter-cellular communication.Journal of the Royal Society of New Zealand · 2023Review
- Neurochemical Anatomy of the Mammalian Carotid Body.Advances in anatomy, embryology, and cell biology · 2023Article
- Resolving the Ionotropic P2X4 Receptor Mystery Points Towards a New Therapeutic Target for Cardiovascular Diseases.International journal of molecular sciences · 2020Review
- Purines and Carotid Body: New Roles in Pathological Conditions.Frontiers in pharmacology · 2017Review
- Synaptic and paracrine mechanisms at carotid body arterial chemoreceptors.The Journal of physiology · 2014Review
- Gasotransmitter regulation of ion channels: a key step in O2 sensing by the carotid body.Physiology (Bethesda, Md.) · 2014Review
- Expanding role of ATP as a versatile messenger at carotid and aortic body chemoreceptors.The Journal of physiology · 2013Review
- Peripheral-central chemoreceptor interaction and the significance of a critical period in the development of respiratory control.Respiratory physiology & neurobiology · 2013Review
- P2Y2 receptor activation opens pannexin-1 channels in rat carotid body type II cells: potential role in amplifying the neurotransmitter ATP.The Journal of physiology · 2012Article
- Effects of chemostimuli on [Ca2+]i responses of rat aortic body type I cells and endogenous local neurons: comparison with carotid body cells.The Journal of physiology · 2012Article
- Peripheral chemoreceptors: function and plasticity of the carotid body.Comprehensive Physiology · 2012Review
- Carotid body function in aged rats: responses to hypoxia, ischemia, dopamine, and adenosine.Age (Dordrecht, Netherlands) · 2011Article
- Role of nitric oxide on purinergic signalling in the cochlea.Purinergic signalling · 2010Article
- Postsynaptic action of GABA in modulating sensory transmission in co-cultures of rat carotid body via GABA(A) receptors.The Journal of physiology · 2009Article
- Purines, the carotid body and respiration.Respiratory physiology & neurobiology · 2007Review
- Increased endogenous nitric oxide release by iron chelation and purinergic activation in the rat carotid body.The open biochemistry journal · 2007Article
- Anatomical and physiological factors contributing to chronic muscle pain.Current topics in behavioral neurosciencesArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, ventilation is peripherally controlled by the carotid body (CB), which receives afferent innervation from the petrosal ganglion and efferent innervation from neurons located along the glossopharyngeal nerve (GPN). GPN neurons give rise to the "efferent inhibitory" pathway via a plexus of neuronal nitric oxide (NO) synthase-positive fibers, believed to be responsible for CB chemoreceptor inhibition via NO release. Although NO is elevated during natural CB stimulation by hypoxia, the underlying mechanisms are unclear. We hypothesized that ATP, released by rat CB chemoreceptors (type 1 cells) and/or red blood cells during hypoxia, may directly activate GPN neurons and contribute to NO-mediated inhibition. Using combined electrophysiological, molecular, and confocal immunofluorescence techniques, we detected the expression of multiple P2X receptors in GPN neurons. These receptors involve at least four different purinergic subunits: P2X2 [and the splice variant P2X2(b)], P2X3, P2X4, and P2X7. Using a novel coculture preparation of CB type I cell clusters and GPN neurons, we tested the role of P2X signaling on CB function. In cocultures, fast application of ATP, or its synthetic analog 2',3'-O-(4 benzoylbenzoyl)-ATP, caused type I cell hyperpolarization that was prevented in the presence of the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide potassium. These data suggest that ATP released during hypoxic stress from CB chemoreceptors (and/or red blood cells) will cause GPN neuron depolarization mediated by multiple P2X receptors. Activation of this pathway will lead to calcium influx and efferent inhibition of CB chemoreceptors via NO synthesis and consequent release.
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