ArticleMolecular pain2014
Voltage-gated sodium channel expression in mouse DRG after SNI leads to re-evaluation of projections of injured fibers.
Article in Molecular pain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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52 citing papers in PubMed, 80 citations in OpenAlex.
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- Preclinical Animal Models to Investigate the Role of NaLife (Basel, Switzerland) · 2025Review
- Dorsal root ganglia CSF1Journal of the peripheral nervous system : JPNS · 2024Article
- Peripherally restricted PICK1 inhibitor mPD5 ameliorates pain behaviors in murine inflammatory and neuropathic pain models.JCI insight · 2024Article
- Sigma-1 Receptors Control Neuropathic Pain and Peripheral Neuroinflammation After Nerve Injury in Female Mice: A Transcriptomic Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- A Perspective on Electrical Stimulation and Sympathetic Regeneration in Peripheral Nerve Injuries.Neurotrauma reports · 2024Article
- NMDA Receptors at Primary Afferent-Excitatory Neuron Synapses Differentially Sustain Chemotherapy- and Nerve Trauma-Induced Chronic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Neat1 lncRNA organizes the inflammatory gene expressions in the dorsal root ganglion in neuropathic pain caused by nerve injury.Frontiers in immunology · 2023Article
- Spinal cord retinoic acid receptor signaling gates mechanical hypersensitivity in neuropathic pain.Neuron · 2022Article
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- Theta-Burst Stimulation of Primary Afferents Drives Long-Term Potentiation in the Spinal Cord and Persistent Pain via α2δ-1-Bound NMDA Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- The Development of Mechanical Allodynia in Diabetic Rats Revealed by Single-Cell RNA-Seq.Frontiers in molecular neuroscience · 2022Article
- Development of a common peroneal nerve injury model in domestic swine for the study of translational neuropathic pain treatments.Journal of neurosurgery · 2021Article
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- Loss of Prdm12 during development, but not in mature nociceptors, causes defects in pain sensation.Cell reports · 2021Article
- Review
- Transcriptional Reprogramming of Distinct Peripheral Sensory Neuron Subtypes after Axonal Injury.Neuron · 2020Article
- The Lipid Receptor G2A (GPR132) Mediates Macrophage Migration in Nerve Injury-Induced Neuropathic Pain.Cells · 2020Article
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4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDysregulation of voltage-gated sodium channels (Na(v)s) is believed to play a major role in nerve fiber hyperexcitability associated with neuropathic pain. A complete transcriptional characterization of the different isoforms of Na(v)s under normal and pathological conditions had never been performed on mice, despite their widespread use in pain research. Na(v)s mRNA levels in mouse dorsal root ganglia (DRG) were studied in the spared nerve injury (SNI) and spinal nerve ligation (SNL) models of neuropathic pain. In the SNI model, injured and non-injured neurons were intermingled in lumbar DRG, which were pooled to increase the tissue available for experiments.
resultsA strong downregulation was observed for every Na(v)s isoform expressed except for Na(v)1.2; even Na(v)1.3, known to be upregulated in rat neuropathic pain models, was lower in the SNI mouse model. This suggests differences between these two species. In the SNL model, where the cell bodies of injured and non-injured fibers are anatomically separated between different DRG, most Na(v)s were observed to be downregulated in the L5 DRG receiving axotomized fibers. Transcription was then investigated independently in the L3, L4 and L5 DRG in the SNI model, and an important downregulation of many Na(v)s isoforms was observed in the L3 DRG, suggesting the presence of numerous injured neurons there after SNI. Consequently, the proportion of axotomized neurons in the L3, L4 and L5 DRG after SNI was characterized by studying the expression of activating transcription factor 3 (ATF3). Using this marker of nerve injury confirmed that most injured fibers find their cell bodies in the L3 and L4 DRG after SNI in C57BL/6 J mice; this contrasts with their L4 and L5 DRG localization in rats. The spared sural nerve, through which pain hypersensitivity is measured in behavioral studies, mostly projects into the L4 and L5 DRG.
conclusionsThe complex regulation of Na(v)s, together with the anatomical rostral shift of the DRG harboring injured fibers in C57BL/6 J mice, emphasize that caution is necessary and preliminary anatomical experiments should be carried out for gene and protein expression studies after SNI in mouse strains.
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