ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Inflammatory pain unmasks heterosynaptic facilitation in lamina I neurokinin 1 receptor-expressing neurons in rat spinal cord.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 53 citations in OpenAlex.
- Sensory plasticity of dorsal horn silent neurons as a critical mechanism for neuropathic pain.Nature communications · 2026Article
- No evidence for homotopic hyperalgesia to C fibre stimulation after transcutaneous high-frequency stimulation in humans.The Journal of physiology · 2026Article
- Methylglyoxal alters C-fibre activity-dependent slowing and induces heat hyperalgesia in a sex-dependent manner, in rats.Pain reports · 2026Article
- LGI3/2-ADAM23 interactions cluster Kv1 channels in myelinated axons to regulate refractory period.The Journal of cell biology · 2023Article
- Pre-Synaptic GABACells · 2022Article
- Heterosynaptic facilitation of mechanical nociceptive input is dependent on the frequency of conditioning stimulation.Journal of neurophysiology · 2019Article
- Endogenous transient receptor potential ankyrin 1 and vanilloid 1 activity potentiates glutamatergic input to spinal lamina I neurons in inflammatory pain.Journal of neurochemistry · 2019Article
- Presynaptic Inhibition of Primary Nociceptive Signals to Dorsal Horn Lamina I Neurons by Dopamine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Melatonin limits paclitaxel-induced mitochondrial dysfunction in vitro and protects against paclitaxel-induced neuropathic pain in the rat.Journal of pineal research · 2017Article
- Inflammatory Pain Reduces C Fiber Activity-Dependent Slowing in a Sex-Dependent Manner, Amplifying Nociceptive Input to the Spinal Cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Slit2/Robo1 Mediation of Synaptic Plasticity Contributes to Bone Cancer Pain.Molecular neurobiology · 2017Article
- The control of alternative splicing by SRSF1 in myelinated afferents contributes to the development of neuropathic pain.Neurobiology of disease · 2016Article
- Gastrodin protects against chronic inflammatory pain by inhibiting spinal synaptic potentiation.Scientific reports · 2016Article
- Article
- Persistent changes in peripheral and spinal nociceptive processing after early tissue injury.Experimental neurology · 2016Review
- Transient, activity dependent inhibition of transmitter release from low threshold afferents mediated by GABAA receptors in spinal cord lamina III/IV.Molecular pain · 2015Article
- Inhibitory Interneurons That Express GFP in the PrP-GFP Mouse Spinal Cord Are Morphologically Heterogeneous, Innervated by Several Classes of Primary Afferent and Include Lamina I Projection Neurons among Their Postsynaptic Targets.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Article
- Synaptic GluN2A and GluN2B containing NMDA receptors within the superficial dorsal horn activated following primary afferent stimulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- The chemerin receptor 23 agonist, chemerin, attenuates monosynaptic C-fibre input to lamina I neurokinin 1 receptor expressing rat spinal cord neurons in inflammatory pain.Molecular pain · 2014Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Central sensitization in inflammatory pain conditions results in behavioral mechanical hypersensitivity. Specifically, C-fiber-driven spinal hyperexcitability enables A fibers to gain access to specific spinal circuitry, via heterosynaptic facilitatory mechanisms, to mediate mechanical hypersensitivity. However, the precise circuitry engaged is not known. Lamina I neurokinin 1 (NK1) receptor expressing (NK1R(+)) dorsal horn neurons, many of which are projection neurons, are required for the development of this hypersensitivity and are therefore likely to be a component of this circuitry. To investigate, whole-cell patch-clamp recordings were made from lamina I NK1R(+) neurons in the spinal cord slice preparation with attached dorsal root, obtained from rats with or without complete Freund's adjuvant (CFA) hindpaw inflammation. EPSCs were recorded in response to electrical stimulation of the dorsal root. Control neurons predominantly received monosynaptic C-fiber input (69%) with a smaller proportion receiving monosynaptic Aδ-fiber input (28%). In contrast, CFA inflammation significantly increased the incidence (by twofold) and magnitude (by 75% in a subset) of monosynaptic Aδ-fiber but not monosynaptic C-fiber-evoked responses. Aβ-fiber input to lamina I NK1R(+) neurons was minimal, polysynaptic in nature, and unaltered by CFA inflammation. Additional examination of control neurons revealed that a proportion received silent monosynaptic Aδ-fiber input, suggesting that these may provide the substrate for the novel Aδ inputs observed in CFA inflammation. This inflammation induced unmasking and strengthening of monosynaptic Aδ drive to lamina I NK1R(+) neurons may contribute to the heterosynaptic facilitatory mechanisms underlying mechanical hyperalgesia in inflammatory pain.
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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.