ArticleEuropean journal of pain (London, England)2011
Vector-mediated release of GABA attenuates pain-related behaviors and reduces Na(V)1.7 in DRG neurons.
Article in European journal of pain (London, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Review
- siRNA Treatments for Diabetic Neuropathy: Obstacles and Delivery Techniques.Current molecular medicine · 2025Review
- Stem Cell Therapy for Modulating Neuroinflammation in Neuropathic Pain.International journal of molecular sciences · 2021Review
- Viral Vector-Mediated Gene Transfer of Glutamic Acid Decarboxylase for Chronic Pain Treatment: A Literature Review.Human gene therapy · 2020Review
- Article
- Mining the NaBiochemical pharmacology · 2019Review
- Gene therapy for neuropathic pain using dorsal root ganglion-targeted helper-dependent adenoviral vectors with GAD67 expression.Pain reports · 2018Article
- Roles of Voltage-Gated Tetrodotoxin-Sensitive Sodium Channels NaV1.3 and NaV1.7 in Diabetes and Painful Diabetic Neuropathy.International journal of molecular sciences · 2016Review
- HSV vector-mediated GAD67 suppresses neuropathic pain induced by perineural HIV gp120 in rats through inhibition of ROS and Wnt5a.Gene therapy · 2016Article
- Sodium channel Nav1.7 expression is upregulated in the dorsal root ganglia in a rat model of paclitaxel-induced peripheral neuropathy.SpringerPlus · 2016Article
- Current gene therapy using viral vectors for chronic pain.Molecular pain · 2015Review
- Attenuation of myogenic orofacial nociception and mechanical hypersensitivity by viral mediated enkephalin overproduction in male and female rats.BMC neurology · 2015Article
- The role of sodium channels in painful diabetic and idiopathic neuropathy.Current diabetes reports · 2014Review
- 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
- Herpes simplex virus-based nerve targeting gene therapy in pain management.Journal of pain research · 2014Review
- Comparative effectiveness of antinociceptive gene therapies in animal models of diabetic neuropathic pain.Gene therapy · 2013Article
- Progress in gene therapy for neurological disorders.Nature reviews. Neurology · 2013Review
- The Na(V)1.7 sodium channel: from molecule to man.Nature reviews. Neuroscience · 2013Review
- Gene therapy for the treatment of chronic peripheral nervous system pain.Neurobiology of disease · 2012Review
- Reduction of voltage gated sodium channel protein in DRG by vector mediated miRNA reduces pain in rats with painful diabetic neuropathy.Molecular pain · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Pain is a common and debilitating accompaniment of neuropathy that occurs as a complication of diabetes. In the current study, we examined the effect of continuous release of gamma amino butyric acid (GABA), achieved by gene transfer of glutamic acid decarboxylase (GAD67) to dorsal root ganglia (DRG) in vivo using a non-replicating herpes simplex virus (HSV)-based vector (vG) in a rat model of painful diabetic neuropathy (PDN). Subcutaneous inoculation of vG reduced mechanical hyperalgesia, thermal hyperalgesia and cold allodynia in rats with PDN. Continuous release of GABA from vector transduced cells in vivo prevented the increase in the voltage-gated sodium channel isoform 1.7 (Na(V)1.7) protein that is characteristic of PDN. In vitro, infection of primary DRG neurons with vG prevented the increase in Na(V)1.7 resulting from exposure to hyperglycemia. The effect of vector-mediated GABA on Na(V)1.7 levels in vitro was blocked by phaclofen but not by bicuculline, a GABA(B) receptor effect that was blocked by pertussis toxin-(PTX) interference with Gα((i/o)) function. Taken in conjunction with our previous observation that continuous activation of delta opioid receptors by vector-mediated release of enkephalin also prevents the increase in Na(V)1.7 in DRG exposed to hyperglycemia in vitro or in vivo, the observations in this report suggest a novel common mechanism through which activation of G protein coupled receptors (GPCR) in DRG neurons regulate the phenotype of the primary afferent.
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Registered trials
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