ArticleThe Journal of biological chemistry2011
Nitric oxide inhibits nociceptive transmission by differentially regulating glutamate and glycine release to spinal dorsal horn neurons.
Article in The Journal of biological chemistry, 2011. 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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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Bioguided Isolation of (Pharmaceutics · 2026Article
- Nitric oxide synthase activation in nTS is essential to NMDA receptor dependent encoding of the cough reflex.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- Extracorporeal Shockwave Therapy in Pain Management - an In-Depth Narrative Review.Orthopedic reviews · 2026Article
- Spinal glycine receptor alpha 1 coordinates startle behavior through a cell-type specific mechanism.International journal of biological sciences · 2026Article
- Tonic GABA and Glycine Inhibition Control Pain Hypersensitivity via Limiting α2δ-1- and mGluR5-Dependent NMDA Receptor Activity at Primary Afferent→Excitatory Neuron Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Critical periods inFrontiers in physiology · 2022Review
- Neuromeric Distribution of Nicotinamide Adenine Dinucleotide Phosphate-Diaphorase Activity in the Adult Lamprey Brain.Frontiers in neuroanatomy · 2022Article
- Nitric oxide signalling in the brain and its control of bodily functions.British journal of pharmacology · 2020Review
- Methanol Extract ofBiomolecules · 2020Article
- Contralateral monoarthritis exacerbated chronic constriction injury-induced pain hypersensitivity through upregulating inducible nitric oxide synthase.Journal of pain research · 2018Article
- Endogenous nitric oxide inhibits spinal NMDA receptor activity and pain hypersensitivity induced by nerve injury.Neuropharmacology · 2017Article
- Transmission pathways and mediators as the basis for clinical pharmacology of pain.Expert review of clinical pharmacology · 2016Article
- Dysregulation of Neuronal Ca2+ Channel Linked to Heightened Sympathetic Phenotype in Prohypertensive States.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Molecular Basis of Regulating High Voltage-Activated Calcium Channels by S-Nitrosylation.The Journal of biological chemistry · 2015Article
- Herpes simplex virus vector-mediated gene transfer of kynurenine aminotransferase improves detrusor overactivity in spinal cord-injured rats.Gene therapy · 2014Article
- Casein kinase II inhibition reverses pain hypersensitivity and potentiated spinal N-methyl-D-aspartate receptor activity caused by calcineurin inhibitor.The Journal of pharmacology and experimental therapeutics · 2014Article
- Article
- Distinct intrinsic and synaptic properties of pre-sympathetic and pre-parasympathetic output neurons in Barrington's nucleus.Journal of neurochemistry · 2013Article
- The nitroxyl donor, Angeli's salt, inhibits inflammatory hyperalgesia in rats.Neuropharmacology · 2013Article
- Nitric oxide modulated the expression of DREAM/calsenilin/KChIP3 in inflammatory pain of rats.Inflammation · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO) is involved in many physiological functions, but its role in pain signaling remains uncertain. Surprisingly, little is known about how endogenous NO affects excitatory and inhibitory synaptic transmission at the spinal level. Here we determined how NO affects excitatory and inhibitory synaptic inputs to dorsal horn neurons using whole-cell recordings in rat spinal cord slices. The NO precursor L-arginine or the NO donor SNAP significantly increased the frequency of glycinergic spontaneous and miniature inhibitory postsynaptic currents (IPSCs) of lamina II neurons. However, neither L-arginine nor SNAP had any effect on GABAergic IPSCs. L-arginine and SNAP significantly reduced the amplitude of monosynaptic excitatory postsynaptic currents (EPSCs) evoked from the dorsal root with an increase in paired-pulse ratio. Inhibition of the soluble guanylyl cyclase abolished the effect of L-arginine on glycinergic IPSCs but not on evoked monosynaptic EPSCs. Also, inhibition of protein kinase G blocked the increase in glycinergic sIPSCs by the cGMP analog 8-bromo-cGMP. The inhibitory effects of L-arginine on evoked EPSCs and high voltage-activated Ca(2+) channels expressed in HEK293 cells and dorsal root ganglion neurons were abolished by blocking the S-nitrosylation reaction with N-ethylmaleimide. Intrathecal injection of L-arginine and SNAP significantly increased mechanical nociceptive thresholds. Our findings suggest that spinal endogenous NO enhances inhibitory glycinergic input to dorsal horn neurons through sGC-cGMP-protein kinase G. Furthermore, NO reduces glutamate release from primary afferent terminals through S-nitrosylation of voltage-activated Ca(2+) channels. Both of these actions probably contribute to inhibition of nociceptive transmission by NO at the spinal level.
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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.