ArticleThe Journal of pharmacology and experimental therapeutics2013
Nerve injury increases GluA2-lacking AMPA receptor prevalence in spinal cords: functional significance and signaling mechanisms.
Article in The Journal of pharmacology and experimental therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
- AMPA receptor, neuroimaging, and chronic pain.Journal of anesthesia · 2026Review
- Article
- New insight into RNA biomarkers in neuropathic pain: a clinician-neuroscientist roadmap to translational testing and treatment monitoring a clinical review.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- Electroactive biomaterials modulating ion channels in nervous system regeneration.Regenerative biomaterials · 2026Review
- α2δ-1-Linked NMDA and AMPA Receptors in Neuropathic Pain and Gabapentinoid Action.Journal of neurochemistry · 2025Review
- AMPAR Regulation in Synaptic Plasticity: The Roles of Calcineurin, CK2, and α2δ-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Spinal Cord Stimulation for Spinal Cord Injury-Related Pain: A Pilot Study.Brain sciences · 2024Article
- AMPA and NMDA Receptors in Hippocampus of Rats with Fluoride-Induced Cognitive Decline.International journal of molecular sciences · 2024Article
- Article
- Calcineurin and CK2 Reciprocally Regulate Synaptic AMPA Receptor Phenotypes via α2δ-1 in Spinal Excitatory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Sex differences in pre- and post-synaptic glutamate signaling in the nucleus accumbens core.Biology of sex differences · 2023Article
- Sex differences in the medial prefrontal cortical glutamate system.Biology of sex differences · 2022Article
- δ-Opioid receptors in primary sensory neurons tonically restrain nociceptive input in chronic pain but do not enhance morphine analgesic tolerance.Neuropharmacology · 2022Article
- 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
- Spinal AMPA receptors: Amenable players in central sensitization for chronic pain therapy?Channels (Austin, Tex.) · 2021Review
- AKAP150 and its Palmitoylation Contributed to Pain Hypersensitivity Via Facilitating Synaptic Incorporation of GluA1-Containing AMPA Receptor in Spinal Dorsal Horn.Molecular neurobiology · 2021Article
- α2δ-1 switches the phenotype of synaptic AMPA receptors by physically disrupting heteromeric subunit assembly.Cell reports · 2021Article
- Calcium Permeable-AMPA Receptors and Excitotoxicity in Neurological Disorders.Frontiers in neural circuits · 2021Review
- A Novel Peripheral Action of PICK1 Inhibition in Inflammatory Pain.Frontiers in cellular neuroscience · 2021Article
- Sequential Activation of AMPA Receptors and Glial Cells in a Pain Model of Lumbar Spine Disc Herniation.Annals of rehabilitation medicine · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs) are critically involved in the excitatory synaptic transmission, and blocking AMPARs at the spinal level reverses neuropathic pain. However, little is known about changes in the composition of synaptic AMPARs in the spinal dorsal horn after peripheral nerve injury. AMPARs lacking the GluA2 subunit are permeable to Ca(2+), and their currents show unique inward rectification. We found that AMPAR-mediated excitatory postsynaptic currents (AMPAR-EPSCs) of spinal dorsal horn neurons exhibited a linear current-voltage relationship in control rats, whereas AMPAR-EPSCs of dorsal horn neurons displayed inward rectification in rats with spinal nerve injury. In nerve-injured rats, compared with control rats, the GluA2 protein level was significantly less in the plasma membrane but was greater in the cytosolic vesicle fraction in the dorsal spinal cord. However, the GluA1 protein levels in these fractions did not differ significantly between nerve-injured and control rats. Blocking N-methyl-d-aspartate receptors (NMDARs) abolished inward rectification of AMPAR-EPSCs of dorsal horn neurons in nerve-injured rats. Furthermore, inhibition of calpain or calcineurin, but not protein kinase C, completely blocked nerve injury-induced inward rectification of AMPAR-EPSCs of dorsal horn neurons. In addition, blocking GluA2-lacking AMPARs at the spinal cord level reduced nerve injury-induced pain hypersensitivity. Our study suggests that nerve injury increases GluA2 internalization and the prevalence of GluA2-lacking AMPARs in the spinal dorsal horn to maintain chronic neuropathic pain. Increased prevalence of spinal GluA2-lacking AMPARs in neuropathic pain is mediated by NMDARs and subsequent stimulation of calpain and calcineurin signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.