ReviewHandbook of experimental pharmacology2015
The pharmacology of nociceptor priming.
Review in Handbook of experimental pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed.
- Inflammatory neuropathy in mouse and primate models of colorectal cancer.Nature communications · 2026Article
- MASSAG model: Towards an integrative neuroscience framework linking emotional trauma, pain, and mechanisms of force-based manipulations.Neuroscience and biobehavioral reviews · 2026Review
- Cdk5 modulates orofacial pain through P2X2/3 purinergic receptor-mediated signaling in trigeminal neurons.Frontiers in pharmacology · 2026Article
- GPR37 activation erases spinal pain memory and resolves increased nociception in murine models.bioRxiv : the preprint server for biology · 2025Article
- Metabolic reprogramming in the spinal cord drives the transition to pain chronicity.Cell reports · 2025Article
- Metabolic reprogramming in the spinal cord drives the transition to pain chronicity.bioRxiv : the preprint server for biology · 2025Article
- Mechanism-based nonopioid analgesic targets.The Journal of clinical investigation · 2025Review
- Article
- Plasticity of Mouse Dorsal Root Ganglion Neurons by Innate Immune Activation Is Influenced by Electrophysiological Activity.Journal of neurochemistry · 2025Article
- Upregulation of delta opioid receptor by meningeal interleukin-10 prevents relapsing pain.Brain, behavior, and immunity · 2025Article
- Mu-Opioid Receptor (MOR) Dependence of Pain in Chemotherapy-Induced Peripheral Neuropathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Exploring the role of spinal astrocytes in the onset of hyperalgesic priming signals in acid-induced chronic muscle pain.PNAS nexus · 2024Article
- Peripheral macrophages contribute to nociceptor priming in mice with chronic intermittent hypoxia.Science signaling · 2024Article
- Brain-Derived Neurotrophic Factor, Nociception, and Pain.Biomolecules · 2024Review
- NAAA-regulated lipid signaling in monocytes controls the induction of hyperalgesic priming in mice.Nature communications · 2024Article
- Widespread latent hyperactivity of nociceptors outlasts enhanced avoidance behavior following incision injury.bioRxiv : the preprint server for biology · 2024Article
- Inflammation-induced mitochondrial and metabolic disturbances in sensory neurons control the switch from acute to chronic pain.Cell reports. Medicine · 2023Article
- Identification of brain areas in mice with peak neural activity across the acute and persistent phases of post-traumatic headache.Cephalalgia : an international journal of headache · 2023Article
- C781, a β-Arrestin Biased Antagonist at Protease-Activated Receptor-2 (PAR2), Displays in vivo Efficacy Against Protease-Induced Pain in Mice.The journal of pain · 2023Article
- Predictive analytics identifies key factors driving hyperalgesic priming of muscle sensory neurons.Frontiers in neuroscience · 2023Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Nociceptors and neurons in the central nervous system (CNS) that receive nociceptive input show remarkable plasticity in response to injury. This plasticity is thought to underlie the development of chronic pain states. Hence, further understanding of the molecular mechanisms driving and maintaining this plasticity has the potential to lead to novel therapeutic approaches for the treatment of chronic pain states. An important concept in pain plasticity is the presence and persistence of "hyperalgesic priming." This priming arises from an initial injury and results in a remarkable susceptibility to normally subthreshold noxious inputs causing a prolonged pain state in primed animals. Here we describe our current understanding of how this priming is manifested through changes in signaling in the primary nociceptor as well as through memory like alterations at CNS synapses. Moreover, we discuss how commonly utilized analgesics, such as opioids, enhance priming therefore potentially contributing to the development of persistent pain states. Finally we highlight where these priming models draw parallels to common human chronic pain conditions. Collectively, these advances in our understanding of pain plasticity reveal a variety of targets for therapeutic intervention with the potential to reverse rather than palliate chronic 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.