ArticleMolecular pain2010
Expression of inwardly rectifying potassium channels by an inducible adenoviral vector reduced the neuronal hyperexcitability and hyperalgesia produced by chronic compression of the spinal ganglion.
Article in Molecular pain, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Multi-omic profiling of human and mouse dorsal root ganglia enables targeted gene delivery to nociceptors.bioRxiv : the preprint server for biology · 2026Article
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- Regulation of pain neurotransmitters and chondrocytes metabolism mediated by voltage-gated ion channels: A narrative review.Heliyon · 2023Review
- Neuronal C-Reactive Protein/FcγRI Positive Feedback Proinflammatory Signaling Contributes to Nerve Injury Induced Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Distinct Gene Expression Patterns of Ion Channels and Cytokines in Rat Primary Sensory Neurons During Development of Bone Cancer and Cancer Pain.Frontiers in molecular neuroscience · 2021Article
- Kir2.1 Channel Regulation of Glycinergic Transmission Selectively Contributes to Dynamic Mechanical Allodynia in a Mouse Model of Spared Nerve Injury.Neuroscience bulletin · 2019Article
- Article
- Anti-nociceptive effects of bupivacaine-encapsulated PLGA nanoparticles applied to the compressed dorsal root ganglion in mice.Neuroscience letters · 2018Article
- A-Type KFrontiers in molecular neuroscience · 2018Review
- Inward-rectifying KNeuroscience · 2016Article
- G9a is essential for epigenetic silencing of K(+) channel genes in acute-to-chronic pain transition.Nature neuroscience · 2015Article
- Increase in the titer of lentiviral vectors expressing potassium channels by current blockade during viral vector production.BMC neuroscience · 2015Article
- Opening paths to novel analgesics: the role of potassium channels in chronic pain.Trends in neurosciences · 2014Review
- Sympathectomy attenuates excitability of dorsal root ganglion neurons and pain behaviour in a lumbar radiculopathy model.Bone & joint research · 2012Article
- Chronic nerve compression alters Schwann cell myelin architecture in a murine model.Muscle & nerve · 2012Article
- Direct injection into the dorsal root ganglion: technical, behavioral, and histological observations.Journal of neuroscience methods · 2011Article
- Article
- Satellite glial cells in the trigeminal ganglion as a determinant of orofacial neuropathic pain.Neuron glia biology · 2006Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundA chronic compressed dorsal root ganglion (CCD) in rat produces pain behavior and an enhanced excitability of neurons within the compressed ganglion. Kir2.1 is an inwardly rectifying potassium channel that acts to stabilize the resting potential of certain cell types. We hypothesized that an inducible expression of Kir2.1 channels in CCD neurons might suppress neuronal excitability in the dorsal root ganglion (DRG) and reduce the associated pain behavior.
resultsWe delivered, by microinjection into the fourth lumbar (L4) DRG, an adenoviral vector containing a reporter gene encoding the enhanced green fluorescent protein (GFP) and a Kir2.1 channel (AdKir). At the same time the ganglion was compressed by implantation of a rod through the intervertebral foramen (CCD). The in vivo expression of the transferred gene was controlled by an ecdysone analog via an ecdysone-inducible promoter in the viral vector. In comparison with the effects of vehicle or a control vector containing only the GFP gene, AdKir significantly reduced the neuronal hyperexcitability after CCD. Electrophysiological recordings, in vivo, from nociceptive and non-nociceptive DRG neurons expressing the virally produced Kir2.1 channels revealed a hyperpolarized resting membrane potential, an increased rheobase, and lack of spontaneous activity. Inducing the Kir2.1 gene at the beginning of CCD surgery partially prevented the development of mechanical hyperalgesia. However, a delayed induction of the Kir2.1 gene (3 days after CCD surgery) produced no significant effect on the pain behavior.
conclusionsWe found that an inducible expression of Kir2.1 channels in chronically compressed DRG neurons can effectively suppress the neuronal excitability and, if induced at the beginning of CCD injury, prevent the development of hyperalgesia. We hypothesize that a higher level of neuronal hyperexcitability in the DRG is required to initiate than to maintain the hyperalgesia and that the hyperexcitability contributing to neuropathic pain is best inhibited as soon as possible after injury.
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