ArticleMolecular pain2013
Hydrogen sulfide increases excitability through suppression of sustained potassium channel currents of rat trigeminal ganglion neurons.
Article in Molecular pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 39 citations in OpenAlex.
- The Role of Hydrogen Sulfide in Peripheral Nervous System Modulation.Handbook of experimental pharmacology · 2026Review
- The cornea-trigeminal axis: potassium channels as master regulators of ocular surface homeostasis and sensory transduction.Frontiers in cell and developmental biology · 2026Review
- Hydrogen Sulfide Biomedical Research in China-20 Years of Hindsight.Antioxidants (Basel, Switzerland) · 2022Review
- Protective Effects of Hydrogen Sulfide Against the ATP-Induced Meningeal Nociception.Frontiers in cellular neuroscience · 2020Article
- Electrical stimulation of the superior sagittal sinus suppresses A-type KThe journal of headache and pain · 2019Article
- Modulation of KPflugers Archiv : European journal of physiology · 2019Article
- Possible involvement of peripheral TRP channels in the hydrogen sulfide-induced hyperalgesia in diabetic rats.BMC neuroscience · 2019Article
- Hydrogen sulfide inhibits Kir2 and Kir3 channels by decreasing sensitivity to the phospholipid phosphatidylinositol 4,5-bisphosphate (PIPThe Journal of biological chemistry · 2018Article
- GYY4137 Promotes Mice Feeding Behavior via Arcuate Nucleus Sulfur-Sulfhydrylation and AMPK Activation.Frontiers in pharmacology · 2018Article
- Hydrogen sulfide exposure induces NLRP3 inflammasome-dependent IL-1β and IL-18 secretion in human mononuclear leukocytesClinical and experimental dental research · 2017Article
- Electrophysiological Investigation of the Subcellular Fine Tuning of Sympathetic Neurons by Hydrogen Sulfide.Frontiers in pharmacology · 2017Article
- Receptor Mechanisms Mediating the Pro-Nociceptive Action of Hydrogen Sulfide in Rat Trigeminal Neurons and Meningeal Afferents.Frontiers in cellular neuroscience · 2017Article
- Inhibition of cystathionine β-synthetase suppresses sodium channel activities of dorsal root ganglion neurons of rats with lumbar disc herniation.Scientific reports · 2016Article
- Regulation of the T-type Ca(2+) channel Cav3.2 by hydrogen sulfide: emerging controversies concerning the role of H2 S in nociception.The Journal of physiology · 2016Review
- Acute Effects of Transforming Growth Factor-β1 on Neuronal Excitability and Involvement in the Pain of Rats with Chronic Pancreatitis.Journal of neurogastroenterology and motility · 2016Article
- Actions of a hydrogen sulfide donor (NaHS) on transient sodium, persistent sodium, and voltage-gated calcium currents in neurons of the subfornical organ.Journal of neurophysiology · 2015Article
- Sensitization of P2X3 receptors by cystathionine β-synthetase mediates persistent pain hypersensitivity in a rat model of lumbar disc herniation.Molecular pain · 2015Article
- Epigenetic modification of DRG neuronal gene expression subsequent to nerve injury: etiological contribution to complex regional pain syndromes (Part I).Medical science monitor : international medical journal of experimental and clinical research · 2014Review
- Upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint.Molecular pain · 2014Article
- Hydrogen sulfide regulates cardiovascular function by influencing the excitability of subfornical organ neurons.PloS one · 2014Article
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7 authors at 3 institutions in 1 country.
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Abstract
backgroundHydrogen sulfide (H2S), an endogenous gaseotransmitter/modulator, is becoming appreciated that it may be involved in a wide variety of processes including inflammation and nociception. However, the role and mechanism for H2S in nociceptive processing in trigeminal ganglion (TG) neuron remains unknown. The aim of this study is to investigate distribution of endogenous H2S synthesizing enzyme cystathionine-β-synthetase (CBS) expression and role of H2S on excitability and voltage-gated potassium channels of TG neurons.
methodsImmunofluorescence studies were carried out to determine whether CBS was co-expressed in Kv1.1 or Kv1.4-positive TG neurons. Whole cell patch clamp recordings were employed on acutely isolated TG neurons from adult male Sprague Dawley rats (6-8 week old). von Frey filaments were used to examine the pain behavioral responses in rats following injection of sodium hydrosulfide.
resultsIn rat TG, 77.3±6.6% neurons were immunoreactive for CBS, 85.1±3.8% for Kv1.1 and 97.8±1.1% for Kv1.4. Double staining showed that all CBS labeled cells were Kv1.1 and Kv1.4 positive, but only 92.2±6.1% of Kv1.1 and 78.2±9.9% of Kv1.4 positive cells contained CBS. Application of H2S donor NaHS (250 μM) led to a significant depolarization of resting membrane potential recorded from TG neurons. NaHS application also resulted in a dramatic reduction in rheobase, hyperpolarization of action potential threshold, and a significant increase in the number of action potentials evoked at 2X and 3X rheobase stimulation. Under voltage-clamp conditions, TG neurons exhibited transient A-type (IA) and sustained outward rectifier K+ currents (IK). Application of NaHS did suppress IK density while did not change IA density of TG neurons (n=6). Furthermore, NaHS, a donor of hydrogen sulfide, produced a significant reduction in escape threshold in a dose dependent manner.
conclusionThese data suggest that endogenous H2S generating enzyme CBS was co-localized well with Kv1.1 and Kv1.4 in TG neurons and that H2S produces the mechanic pain and increases neuronal excitability, which might be largely mediated by suppressing IK density, thus identifying for the first time a specific molecular mechanism underlying pain and sensitization in TG.
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