ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Spinal dopaminergic projections control the transition to pathological pain plasticity via a D1/D5-mediated mechanism.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 76 citations in OpenAlex.
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- Dopaminergic Dysregulation in Migraine: From Hypothalamic A11 Dysfunction to a Systemic Biobehavioral Phenotype.International journal of molecular sciences · 2026Review
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- Targeting the hypothalamic a11 nucleus to treat parkinsonian-like nociceptive impairments.NPJ Parkinson's disease · 2025Article
- 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
- Effects of perinatal iron deficiency on spinal dorsal horn circuits.The journal of pain · 2025Article
- Sex differences in the transition to chronic pain.The Journal of clinical investigation · 2025Review
- Acetone-Ether-Water Mouse Model of Persistent Itch Fully Resolves Without Latent Pruritic or Cross-Modality Priming.Dermatopathology (Basel, Switzerland) · 2025Article
- Amitriptyline-perphenazine therapy for persistent idiopathic facial pain: translational perspectives from a retrospective study.Journal of anesthesia, analgesia and critical care · 2024Article
- Exploring the role of spinal astrocytes in the onset of hyperalgesic priming signals in acid-induced chronic muscle pain.PNAS nexus · 2024Article
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- Cannabidiol and Tetrahydrocannabinol Antinociceptive Activity is Mediated by Distinct Receptors in Caenorhabditis elegans.Neurochemical research · 2024Article
- Dopaminergic Projections from the Hypothalamic A11 Nucleus to the Spinal Trigeminal Nucleus Are Involved in Bidirectional Migraine Modulation.International journal of molecular sciences · 2023Article
- Descending dopaminergic pathway facilitates itch signal processing via activating spinal GRPREMBO reports · 2023Article
- Early-Life Iron Deficiency Persistently Alters Nociception in Developing Mice.The journal of pain · 2023Article
- Skin-to-skin contact-An effective intervention on pain and stress reduction in preterm infants.Frontiers in pediatrics · 2023Article
- Case report: Methylphenidate improved chronic pain in an adult patient with attention deficit hyperactivity disorder.Frontiers in psychiatry · 2023Article
- Dexamethasone and potassium canrenoate alleviate hyperalgesia by competitively regulating IL-6/JAK2/STAT3 signaling pathway during inflammatory pain in vivo and in vitro.Immunity, inflammation and disease · 2022Article
- Hypothalamic A11 Nuclei Regulate the Circadian Rhythm of Spinal Mechanonociception through Dopamine Receptors and Clock Gene Expression.Life (Basel, Switzerland) · 2022Article
- Evaluation of Urea-Based Inhibitors of the Dopamine Transporter Using the Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis.ACS chemical neuroscience · 2022Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
The mechanisms that lead to the maintenance of chronic pain states are poorly understood, but their elucidation could lead to new insights into how pain becomes chronic and how it can potentially be reversed. We investigated the role of spinal dorsal horn neurons and descending circuitry in plasticity mediating a transition to pathological pain plasticity suggesting the presence of a chronic pain state using hyperalgesic priming. We found that when dorsal horn neurokinin 1 receptor-positive neurons or descending serotonergic neurons were ablated before hyperalgesic priming, IL-6- and carrageenan-induced mechanical hypersensitivity was impaired, and subsequent prostaglandin E2 (PGE2) response was blunted. However, when these neurons were lesioned after the induction of priming, they had no effect on the PGE2 response, reflecting differential mechanisms driving plasticity in a primed state. In stark contrast, animals with a spinally applied dopaminergic lesion showed intact IL-6- and carrageenan-induced mechanical hypersensitivity, but the subsequent PGE2 injection failed to cause mechanical hypersensitivity. Moreover, ablating spinally projecting dopaminergic neurons after the resolution of the IL-6- or carrageenan-induced response also reversed the maintenance of priming as assessed through mechanical hypersensitivity and the mouse grimace scale. Pharmacological antagonism of spinal dopamine D1/D5 receptors reversed priming, whereas D1/D5 agonists induced mechanical hypersensitivity exclusively in primed mice. Strikingly, engagement of D1/D5 coupled with anisomycin in primed animals reversed a chronic pain state, consistent with reconsolidation-like effects in the spinal dorsal horn. These findings demonstrate a novel role for descending dopaminergic neurons in the maintenance of pathological pain plasticity.
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