ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Spinal protein kinase M ζ underlies the maintenance mechanism of persistent nociceptive sensitization.
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 78 papers.
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Who cites it
78 citing papers in PubMed, 123 citations in OpenAlex.
- Persistently Increased Expression of PKMzeta and Unbiased Gene Expression Profiles Identify Hippocampal Molecular Traces of a Long-Term Active Place Avoidance Memory and "Shadow" Proteins.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Persistently increased expression of PKMzeta and unbiased gene expression profiles identify hippocampal molecular traces of a long-term active place avoidance memory and 'shadow' proteins.bioRxiv : the preprint server for biology · 2025Article
- Exploring the role of spinal astrocytes in the onset of hyperalgesic priming signals in acid-induced chronic muscle pain.PNAS nexus · 2024Article
- ephrin-B2 promotes nociceptive plasticity and hyperalgesic priming through EphB2-MNK-eIF4E signaling in both mice and humans.Pharmacological research · 2024Article
- Inflammation-induced mitochondrial and metabolic disturbances in sensory neurons control the switch from acute to chronic pain.Cell reports. Medicine · 2023Article
- Characterization of Fragile X Mental Retardation Protein expression in human nociceptors and their axonal projections to the spinal dorsal horn.The Journal of comparative neurology · 2023Article
- Heterosynaptic long-term potentiation of non-nociceptive synapses requires endocannabinoids, NMDARs, CamKII, and PKCζ.Journal of neurophysiology · 2023Article
- The mechanisms and management of persistent postsurgical pain.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Exchange proteins directly activated by cyclic adenosine monophosphate inhibitor reverses mechanical allodynia via the modification of astrocytes activity in the spinal cord.Annals of translational medicine · 2021Article
- A Novel Peripheral Action of PICK1 Inhibition in Inflammatory Pain.Frontiers in cellular neuroscience · 2021Article
- Increased Pain Symptomatology Among Females vs. Males With Fragile X-Associated Tremor/Ataxia Syndrome.Frontiers in psychiatry · 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
- Blockade of BDNF signalling attenuates chronic visceral hypersensitivity in an IBS-like rat model.European journal of pain (London, England) · 2020Article
- Indirect AMP-Activated Protein Kinase Activators Prevent Incision-Induced Hyperalgesia and Block Hyperalgesic Priming, Whereas Positive Allosteric Modulators Block Only Priming in Mice.The Journal of pharmacology and experimental therapeutics · 2019Article
- Spinal and afferent PKC signaling mechanisms that mediate chronic pain in sickle cell disease.Neuroscience letters · 2019Review
- PKMζ Is Not Required for Development of Postsurgical Pain.Molecular neurobiology · 2018Article
- Article
- Translational Control Mechanisms in Persistent Pain.Trends in neurosciences · 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
- eIF4E-Dependent Translational Control: A Central Mechanism for Regulation of Pain Plasticity.Frontiers in genetics · 2018Review
18 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Sensitization of the pain pathway is believed to promote clinical pain disorders. We hypothesized that the persistence of a sensitized state in the spinal dorsal horn might depend on the activity of protein kinase M ζ (PKMζ), an essential mechanism of late long-term potentiation (LTP). To test this hypothesis, we used intraplantar injections of interleukin-6 (IL-6) in mice to elicit a transient allodynic state that endured ∼3 d. After the resolution of IL-6-induced allodynia, a subsequent intraplantar injection of prostaglandin E(2) (PGE(2)) or intrathecal injection of the metabotropic glutamate receptor 1/5 (mGluR1/5) agonist DHPG (dihydroxyphenylglycol) precipitated allodynia and/or nocifensive responses. Intraplantar injection of IL-6 followed immediately by intrathecal injection of a PKMζ inhibitor prevented the expression of subsequent PGE(2)-induced allodynia. Inhibitors of protein translation were effective in preventing PGE(2)-induced allodynia when given immediately after IL-6, but not after the initial allodynia had resolved. In contrast, spinal PKMζ inhibition completely abolished both prolonged allodynia to hindpaw PGE(2) and enhanced nocifensive behaviors evoked by intrathecal mGluR1/5 agonist injection after the resolution of IL-6-induced allodynia. Moreover, spinal PKMζ inhibition prevented the enhanced response to subsequent stimuli following resolution of hypersensitivity induced by plantar incision. The present findings demonstrate that the spinal cord encodes an engram for persistent nociceptive sensitization that is analogous to molecular mechanisms of late LTP and suggest that spinally directed PKMζ inhibitors may offer therapeutic benefit for injury-induced pain states.
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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.