ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Ionic mechanisms underlying inflammatory mediator-induced sensitization of dural afferents.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 69 citations in OpenAlex.
- The Role of Purinergic Mechanisms in the Excitability of Trigeminal Afferents of Rats with Prenatal Hyperhomocysteinemia.Biomolecules · 2025Article
- Prostaglandin E2 depolarises sensory axons in vitro in an ANO1 and Nav1.8 dependent manner.Scientific reports · 2024Article
- Meningeal Mechanisms and the Migraine Connection.Annual review of neuroscience · 2023Review
- Inhibiting neuronal AC1 for treating anxiety and headache in the animal model of migraine.iScience · 2023Article
- Contribution of tetrodotoxin-resistant persistent NaThe journal of headache and pain · 2022Article
- Molecular mechanisms underlying the actions of arachidonic acid-derived prostaglandins on peripheral nociception.Journal of neuroinflammation · 2020Review
- Modeling a Nociceptive Neuro-Immune Synapse Activated by ATP and 5-HT in Meninges: Novel Clues on Transduction of Chemical Signals Into Persistent or Rhythmic Neuronal Firing.Frontiers in cellular neuroscience · 2020Article
- Animal models of migraine and experimental techniques used to examine trigeminal sensory processing.The journal of headache and pain · 2019Review
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- From Mechanism to Cure: Renewing the Goal to Eliminate the Disease of Pain.Pain medicine (Malden, Mass.) · 2018Review
- Depolarizing Effectors of Bradykinin Signaling in Nociceptor Excitation in Pain Perception.Biomolecules & therapeutics · 2018Review
- Action Potential Broadening in Capsaicin-Sensitive DRG Neurons from Frequency-Dependent Reduction of Kv3 Current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Voltage-gated NaeLife · 2017Article
- A PTEN-Regulated Checkpoint Controls Surface Delivery of δ Opioid Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Paclitaxel-induced increase in mitochondrial volume mediates dysregulation of intracellular CaCell calcium · 2017Article
- Sensory neuron subpopulation-specific dysregulation of intracellular calcium in a rat model of chemotherapy-induced peripheral neuropathy.Neuroscience · 2015Article
- ASICs as therapeutic targets for migraine.Neuropharmacology · 2015Review
- The properties, distribution and function of Na(+)-Ca(2+) exchanger isoforms in rat cutaneous sensory neurons.The Journal of physiology · 2014Article
- Activation of TRPC channels contributes to OA-NO2-induced responses in guinea-pig dorsal root ganglion neurons.The Journal of physiology · 2014Article
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2 authors at 1 institution in 1 country.
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Abstract
Migraineurs experience debilitating headaches that result from neurogenic inflammation of the dura and subsequent sensitization of dural afferents. Given the importance of inflammatory mediator (IM)-induced dural afferent sensitization to this pain syndrome, the present study was designed to identify ionic mechanisms underlying this process. Trigeminal ganglion neurons from adult female Sprague Dawley rats were acutely dissociated 10-14 d after application of retrograde tracer DiI onto the dura. Modulation of ion channels and changes in excitability were measured in the absence and presence of IMs (in mum: 1 prostaglandin, 10 bradykinin, and 1 histamine) using whole-cell and perforated-patch recordings. Fura-2 was used to assess changes in intracellular Ca(2+). IMs modulated a number of currents in dural afferents, including those both expected and/or previously described [i.e., an increase in tetrodotoxin-resistant voltage-gated Na(+) current (TTX-R I(Na)) and a decrease in voltage-gated Ca(2+) current] as well currents never before described in sensory neurons (i.e., a decrease in a Ca(2+)-dependent K(+) current and an increase in a Cl(-) current), and produced a sustained elevation in intracellular Ca(2+). Although several of these currents, in particular TTX-R I(Na), appear to contribute to the sensitization of dural afferents, the Cl(-) current is the primary mechanism underlying this process. Activation of this current plays a dominant role in the sensitization of dural afferents because of the combination of the density and biophysical properties of TTX-R I(Na), and the high level of intracellular Cl(-) in these neurons. These results suggest novel targets for the development of antimigraine agents.
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