ArticleMolecular pain2011
Accumulation of Kv7.2 channels in putative ectopic transduction zones of mice nerve-end neuromas.
Article in Molecular pain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 25 citations in OpenAlex.
- The structure of sensory afferent compartments in health and disease.Journal of anatomy · 2022Review
- Electrophysiological characterization of ectopic spontaneous discharge in axotomized and intact fibers upon nerve transection: a role in spontaneous pain?Pflugers Archiv : European journal of physiology · 2022Review
- Immunostaining in whole-mount lipid-cleared peripheral nerves and dorsal root ganglia after neuropathy in mice.Scientific reports · 2019Article
- Rethinking the causes of pain in herpes zoster and postherpetic neuralgia: the ectopic pacemaker hypothesis.Pain reports · 2018Review
- M-type KBritish journal of pharmacology · 2018Review
- Targeting Kv7 channels in pain pathways.Oncotarget · 2017Article
- The Role of Kv7/M Potassium Channels in Controlling Ectopic Firing in Nociceptors.Frontiers in molecular neuroscience · 2017Article
- Myelin loss and axonal ion channel adaptations associated with gray matter neuronal hyperexcitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Redox and nitric oxide-mediated regulation of sensory neuron ion channel function.Antioxidants & redox signaling · 2015Review
- A New Regulatory Mechanism for Kv7.2 Protein During Neuropathy: Enhanced Transport from the Soma to Axonal Terminals of Injured Sensory Neurons.Frontiers in cellular neuroscience · 2015Article
- Potassium channels in peripheral pain pathways: expression, function and therapeutic potential.Current neuropharmacology · 2013Article
- Article
- Functional significance of M-type potassium channels in nociceptive cutaneous sensory endings.Frontiers in molecular neuroscience · 2012Article
- Spontaneous excitation patterns computed for axons with injury-like impairments of sodium channels and Na/K pumps.PLoS computational biology · 2012Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundModulation of M-type currents has been proposed as a new strategy for the treatment of neuropathic pain due to their role in regulating neuronal excitability. Using electrophysiological techniques we showed previously that the opening of Kv7 channels with retigabine, blocked ectopic discharges from axotomized fibers but did not alter transduction at intact skin afferents. We hypothesized that after nerve damage, accumulation of Kv7 channels in afferent fibers may increase M-type currents which then acquired a more important role at regulating fiber excitability.
findingsIn this study, we used an immunohistochemical approach to examine patterns of expression of Kv7.2 channels in afferent fibers after axotomy and compared them to patterns of expression of voltage gated Na+ channels (Nav) which are key electrogenic elements in peripheral axons known to accumulate in experimental and human neuromas.Axotomy induced an enlargement and narrowing of the nodes of Ranvier at the proximal end of the neuroma together with a dramatic demyelination and loss of structure at its distal end in which naked accumulations of Nav were present. In addition, axotomy also induced accumulations of Kv7.2 that co-localized with those of Nav channels.
conclusionsWhilst Nav channels are mandatory for initiation of action potentials, (i.e. responsible for the generation/propagation of ectopic discharges) an increased accumulation of Kv7.2 channels after axotomy may represent a homeostatic compensation to over excitability in axotomized fibers, opening a window for a peripheral action of M-current modulators under conditions of neuropathy.
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