ArticlePain2015
Induction of long-term potentiation and long-term depression is cell-type specific in the spinal cord.
Article in Pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Human surrogate models of central sensitization: A critical review and practical guide.European journal of pain (London, England) · 2021Pooled it
- Targeting Spinal Dorsal Horn Sensitisation in Chronic Pain: Mechanisms and Translational Strategies.Neuroscience bulletin · 2026Review
- Alternative splicing plasticity of the neurexin family of synaptic adhesion molecules in human sensory neurons.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms and Cell Type-Dependence of Non-Hebbian Long-Term Potentiation at Primary Afferent Synapses in the Mouse Spinal Superficial Dorsal Horn.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Synaptic plasticity in affective comorbidities of neuropathic pain: a bibliometric analysis based on WoSCC and PubMed (2003-2025).Frontiers in neurology · 2026Article
- GPR37 activation erases spinal pain memory and resolves increased nociception in murine models.bioRxiv : the preprint server for biology · 2025Article
- Cannabigerol Modulates Cannabinoid Receptor Type 2 Expression in the Spinal Dorsal Horn and Attenuates Neuropathic Pain Models.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Review
- Cell Type-Dependent Short-Term Plasticity and Dopaminergic Modulation of Sensory Synapses onto Mouse Superficial Dorsal Horn Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Enhancing Functional Recovery After Spinal Cord Injury Through Neuroplasticity: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Effects of Corticosterone on the Excitability of Glutamatergic and GABAergic Neurons of the Adolescent Mouse Superficial Dorsal Horn.Neuroscience · 2023Article
- CaInternational journal of molecular sciences · 2023Article
- Long-term bilateral change in pain and sensitivity to high-frequency cutaneous electrical stimulation in healthy subjects depends on stimulus modality: a dermatomal examination.Frontiers in medicine · 2023Article
- Intensity-dependent modulation of cortical somatosensory processing during external, low-frequency peripheral nerve stimulation in humans.Journal of neurophysiology · 2022Article
- D1/D5 Dopamine Receptors and mGluR5 Jointly Enable Non-Hebbian Long-Term Potentiation at Sensory Synapses onto Lamina I Spinoparabrachial Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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
- NMDARs mediate peripheral and central sensitization contributing to chronic orofacial pain.Frontiers in cellular neuroscience · 2022Review
- Neuron Type-Dependent Synaptic Activity in the Spinal Dorsal Horn of Opioid-Induced Hyperalgesia Mouse Model.Frontiers in synaptic neuroscience · 2021Article
- Mechanisms of Peripheral and Central Pain Sensitization: Focus on Ocular Pain.Frontiers in pharmacology · 2021Review
- MicroRNA profiling of the pig periaqueductal grey (PAG) region reveals candidates potentially related to sex-dependent differences.Biology of sex differences · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The underlying mechanism of chronic pain is believed to be changes in excitability in spinal dorsal horn (DH) neurons that respond abnormally to peripheral input. Increased excitability in pain transmission neurons, and depression of inhibitory neurons, are widely recognized in the spinal cord of animal models of chronic pain. The possible occurrence of 2 parallel but opposing forms of synaptic plasticity, long-term potentiation (LTP) and long-term depression (LTD) was tested in 2 types of identified DH neurons using whole-cell patch-clamp recordings in mouse spinal cord slices. The test stimulus was applied to the sensory fibers to evoke excitatory postsynaptic currents in identified spinothalamic tract neurons (STTn) and GABAergic neurons (GABAn). Afferent conditioning stimulation (ACS) applied to primary afferent fibers with various stimulation parameters induced LTP in STTn but LTD in GABAn, regardless of stimulation parameters. These opposite responses were further confirmed by simultaneous dual patch-clamp recordings of STTn and GABAn from a single spinal cord slice. Both the LTP in STTn and the LTD in GABAn were blocked by an NMDA receptor antagonist, AP5, or an intracellular Ca chelator, BAPTA. Both the pattern and magnitude of intracellular Ca after ACS were almost identical between STTn and GABAn based on live-cell calcium imaging. The results suggest that the intense sensory input induces an NMDA receptor-dependent intracellular Ca increase in both STTn and GABAn, but produces opposing synaptic plasticity. This study shows that there is cell type-specific synaptic plasticity in the spinal DH.
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What OpenQuestion holds
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.