ArticlePain2016
Neuroligin 2 regulates spinal GABAergic plasticity in hyperalgesic priming, a model of the transition from acute to chronic pain.
Article in Pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Neuroligins and Neuropathic Pain: Insights into Synaptic Plasticity and Pain Transmission.Biology · 2026Review
- Neuroligin-2-Dependent Adhesion Defines a Molecular Checkpoint for Inhibitory Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Perturbed synaptic adhesion molecules signaling in neurodevelopmental disorders: The impact of metal neurotoxicity.Ibrain · 2025Review
- Exploring the role of spinal astrocytes in the onset of hyperalgesic priming signals in acid-induced chronic muscle pain.PNAS nexus · 2024Article
- Neuroligin 2 governs synaptic morphology and function through RACK1-cofilin signaling in Drosophila.Communications biology · 2023Article
- Electroacupuncture ameliorates pain in cervical spondylotic radiculopathy rat by inhibiting the CaMKII/CREB/BDNF signaling pathway and regulating spinal synaptic plasticity.Brain and behavior · 2023Article
- Review
- Role of GABAAR in the Transition From Acute to Chronic Pain and the Analgesic Effect of Electroacupuncture on Hyperalgesic Priming Model Rats.Frontiers in neuroscience · 2021Article
- Electroacupuncture Regulates Pain Transition Through Inhibiting PKCε and TRPV1 Expression in Dorsal Root Ganglion.Frontiers in neuroscience · 2021Article
- Clinical Relevance and Prognostic Value of the Neuronal Protein Neuroligin 2 in Breast Cancer.Frontiers in oncology · 2021Article
- Neuroendocrine Mechanisms Governing Sex Differences in Hyperalgesic Priming Involve Prolactin Receptor Sensory Neuron Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Hemokinin-1 Gene Expression Is Upregulated in Trigeminal Ganglia in an Inflammatory Orofacial Pain Model: Potential Role in Peripheral Sensitization.International journal of molecular sciences · 2020Article
- Frameshift mutations at the C-terminus of HIST1H1E result in a specific DNA hypomethylation signature.Clinical epigenetics · 2020Article
- Does epigenetic 'memory' of early-life stress predispose to chronic pain in later life? A potential role for the stress regulatorPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- Changes in Synaptic Proteins Precede Neurodegeneration Markers in Preclinical Alzheimer's Disease Cerebrospinal Fluid.Molecular & cellular proteomics : MCP · 2019Article
- Ketamine differentially restores diverse alterations of neuroligins in brain regions in a rat model of neuropathic pain-induced depression.Neuroreport · 2018Article
- Subliminal (latent) processing of pain and its evolution to conscious awareness.Neuroscience and biobehavioral reviews · 2018Review
- A Critical Role for Dopamine D5 Receptors in Pain Chronicity in Male Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Low GRK2 Underlies Hyperalgesic Priming by Glial Cell-Derived Neurotrophic Factor.Frontiers in pharmacology · 2018Article
- Loss of Neuroligin3 specifically downregulates retinal GABAAα2 receptors without abolishing direction selectivity.PloS one · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Plasticity in inhibitory receptors, neurotransmission, and networks is an important mechanism for nociceptive signal amplification in the spinal dorsal horn. We studied potential changes in GABAergic pharmacology and its underlying mechanisms in hyperalgesic priming, a model of the transition from acute to chronic pain. We find that while GABAA agonists and positive allosteric modulators reduce mechanical hypersensitivity to an acute insult, they fail to do so during the maintenance phase of hyperalgesic priming. In contrast, GABAA antagonism promotes antinociception and a reduction in facial grimacing after the transition to a chronic pain state. During the maintenance phase of hyperalgesic priming, we observed increased neuroligin (nlgn) 2 expression in the spinal dorsal horn. This protein increase was associated with an increase in nlgn2A splice variant mRNA, which promotes inhibitory synaptogenesis. Disruption of nlgn2 function with the peptide inhibitor, neurolide 2, produced mechanical hypersensitivity in naive mice but reversed hyperalgesic priming in mice previously exposed to brain-derived neurotrophic factor. Neurolide 2 treatment also reverses the change in polarity in GABAergic pharmacology observed in the maintenance of hyperalgesic priming. We propose that increased nlgn2 expression is associated with hyperalgesic priming where it promotes dysregulation of inhibitory networks. Our observations reveal new mechanisms involved in the spinal maintenance of a pain plasticity and further suggest that disinhibitory mechanisms are central features of neuroplasticity in the spinal dorsal horn.
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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.