ArticleProceedings of the National Academy of Sciences of the United States of America1999
Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 116 citations in OpenAlex.
- Gut distension evokes rapid neural dynamics in vagal and hindbrain populations of larval zebrafish.iScience · 2026Article
- A small, computationally flexible network produces the phenotypic diversity of song recognition in crickets.eLife · 2021Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Article
- A biophysically detailed computational model of urinary bladder small DRG neuron soma.PLoS computational biology · 2018Article
- Profiling of G protein-coupled receptors in vagal afferents reveals novel gut-to-brain sensing mechanisms.Molecular metabolism · 2018Article
- Depolarizing Effectors of Bradykinin Signaling in Nociceptor Excitation in Pain Perception.Biomolecules & therapeutics · 2018Review
- Vagal Afferent Innervation of the Airways in Health and Disease.Physiological reviews · 2016Review
- Peripheral neural circuitry in cough.Current opinion in pharmacology · 2015Review
- Article
- Article
- Role of prostaglandin D2 in mast cell activation-induced sensitization of esophageal vagal afferents.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Store-operated calcium entry in vagal sensory nerves is independent of Orai channels.Brain research · 2013Article
- Reductions in external divalent cations evoke novel voltage-gated currents in sensory neurons.PloS one · 2012Article
- The anti-botulism triterpenoid toosendanin elicits calcium increase and exocytosis in rat sensory neurons.Cellular and molecular neurobiology · 2011Article
- Subtype-specific reduction of voltage-gated calcium current in medium-sized dorsal root ganglion neurons after painful peripheral nerve injury.Neuroscience · 2011Article
- Inhibition of the plasma membrane Ca2+ pump by CD44 receptor activation of tyrosine kinases increases the action potential afterhyperpolarization in sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Mechanisms of Broad-Spectrum Antiemetic Efficacy of Cannabinoids against Chemotherapy-Induced Acute and Delayed Vomiting.Pharmaceuticals (Basel, Switzerland) · 2010Review
- Ionic mechanisms underlying inflammatory mediator-induced sensitization of dural afferents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Pranlukast prevents cysteinyl leukotriene-induced emesis in the least shrew (Cryptotis parva).European journal of pharmacology · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Activation of distinct classes of potassium channels can dramatically affect the frequency and the pattern of neuronal firing. In a subpopulation of vagal afferent neurons (nodose ganglion neurons), the pattern of impulse activity is effectively modulated by a Ca2+-dependent K+ current. This current produces a post-spike hyperpolarization (AHPslow) that plays a critical role in the regulation of membrane excitability and is responsible for spike-frequency accommodation in these neurons. Inhibition of the AHPslow by a number of endogenous autacoids (e.g., histamine, serotonin, prostanoids, and bradykinin) results in an increase in the firing frequency of vagal afferent neurons from <0.1 to >10 Hz. After a single action potential, the AHPslow in nodose neurons displays a slow rise time to peak (0.3-0.5 s) and a long duration (3-15 s). The slow kinetics of the AHPslow are due, in part, to Ca2+ discharge from an intracellular Ca2+-induced Ca2+ release (CICR) pool. Action potential-evoked Ca2+ influx via either L or N type Ca2+ channels triggers CICR. Surprisingly, although L type channels generate 60% of action potential-induced CICR, only Ca2+ influx through N type Ca2+ channels can trigger the CICR-dependent AHPslow. These observations suggest that a close physical proximity exists between endoplasmic reticulum ryanodine receptors and plasma membrane N type Ca2+ channels and AHPslow potassium channels. Such an anatomical relation might be particularly beneficial for modulation of spike-frequency adaptation in vagal afferent neurons.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.