ArticleMolecular brain2015
Dexmedetomidine inhibits Tetrodotoxin-resistant Nav1.8 sodium channel activity through Gi/o-dependent pathway in rat dorsal root ganglion neurons.
Article in Molecular brain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Dexmedetomidine as an adjuvant to local anesthetics in brachial plexus blocks: A meta-analysis of randomized controlled trials.Medicine · 2017Pooled it
- A Review of Alpha-2 Adrenergic Agents Implicated in Opioid Use Disorder.ACS chemical neuroscience · 2026Review
- Progress on the Mechanisms and Neuroprotective Benefits of Dexmedetomidine in Brain Diseases.Brain and behavior · 2024Review
- Suppression of P2X3 receptor-mediated currents by the activation of αCNS neuroscience & therapeutics · 2022Article
- Dexmedetomidine Co-Administered with Lidocaine Decreases Nociceptive Responses and Trigeminal Fos Expression without Motor Dysfunction and Hypotension in a Murine Orofacial Formalin Model.Life (Basel, Switzerland) · 2022Article
- Comparison of epidural dexmedetomidine to fentanyl in reducing ropivacaine dose in Programmed Intermittent Epidural Bolus plus Patient Controlled Epidural Analgesia during labor: A randomized, double-blind, controlled study.Frontiers in medicine · 2022Article
- Electroencephalogram Mechanism of Dexmedetomidine Deepening Sevoflurane Anesthesia.Frontiers in neuroscience · 2022Article
- Growth Differentiation Factor-15 Produces Analgesia by Inhibiting Tetrodotoxin-Resistant Nav1.8 Sodium Channel Activity in Rat Primary Sensory Neurons.Neuroscience bulletin · 2021Article
- Dexmedetomidine Inhibits ASIC ActivityFrontiers in pharmacology · 2021Article
- Effectiveness in Block by Dexmedetomidine of Hyperpolarization-Activated Cation Current, Independent of Its Agonistic Effect on αInternational journal of molecular sciences · 2020Article
- Conserved Expression of Nav1.7 and Nav1.8 Contribute to the Spontaneous and Thermally Evoked Excitability in IL-6 and NGF-Sensitized Adult Dorsal Root Ganglion Neurons In Vitro.Bioengineering (Basel, Switzerland) · 2020Article
- Organ-Protective Effects and the Underlying Mechanism of Dexmedetomidine.Mediators of inflammation · 2020Review
- Article
- Endothelin type A receptors mediate pain in a mouse model of sickle cell disease.Haematologica · 2018Article
- Dexmedetomidine Inhibits Voltage-Gated Sodium Channels viaMediators of inflammation · 2018Article
- Modulation of Nav1.8 by Lysophosphatidic Acid in the Induction of Bone Cancer Pain.Neuroscience bulletin · 2016Article
- α2-Adrenergic Receptor and Isoflurane Modulation of Presynaptic Ca2+ Influx and Exocytosis in Hippocampal Neurons.Anesthesiology · 2016Article
- Activation of protein kinase A in the amygdala modulates anxiety-like behaviors in social defeat exposed mice.Molecular brain · 2016Article
- Mas-Related Gene (Mrg) C Activation Attenuates Bone Cancer Pain via Modulating Gi and NR2B.PloS one · 2016Article
- Cyclic nucleotide signaling in sensory neuron hyperexcitability and chronic pain after nerve injury.Neurobiology of pain (Cambridge, Mass.)Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSystemically administered dexmedetomidine (DEX), a selective α2 adrenergic receptor (α2-AR) agonists, produces analgesia and sedation. Peripherally restricted α2-AR antagonist could block the analgesic effect of systemic DEX on neuropathic pain, with no effect on sedation, indicating peripheral analgesic effect of DEX. Tetrodotoxin-resistant (TTX-R) sodium channel Nav1.8 play important roles in the conduction of nociceptive sensation. Both α2-AR and Nav1.8 are found in small nociceptive DRG neurons. We, therefore, investigated the effects of DEX on the Nav1.8 currents in acutely dissociated small-diameter DRG neurons.
resultsWhole-cell patch-clamp recordings demonstrated that DEX concentration-dependently suppressed TTX-R Nav1.8 currents in small-diameter lumbar DRG neurons. DEX also shifted the steady-state inactivation curves of Nav1.8 in a hyperpolarizing direction and increased the threshold of action potential and decrease electrical and chemical stimuli-evoked firings in small-diameter DRG neurons. The α2-AR antagonist yohimbine or α2A-AR antagonist BRL44408 but not α2B-AR antagonist imiloxan blocked the inhibition of Nav1.8 currents by DEX. Immunohistochemistry results showed that Nav1.8 was predominantly expressed in peripherin-positive small-diameter DRG neurons, and some of them were α2A-AR-positive ones. Our electrophysiological recordings also demonstrated that DEX-induced inhibition of Nav1.8 currents was prevented by intracellular application of G-protein inhibitor GDPβ-s or Gi/o proteins inhibitor pertussis toxin (PTX), and bath application of adenylate cyclase (AC) activator forskolin or membrane-permeable cAMP analogue 8-Bromo-cAMP (8-Br-cAMP). PKA inhibitor Rp-cAMP could mimic DEX-induced inhibition of Nav1.8 currents.
conclusionsWe established a functional link between α2-AR and Nav1.8 in primary sensory neurons utilizing the Gi/o/AC/cAMP/PKA pathway, which probably mediating peripheral analgesia of DEX.
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