ArticleMolecular brain2022
Relief of neuropathic pain by cell-specific manipulation of nucleus accumbens dopamine D1- and D2-receptor-expressing neurons.
Article in Molecular brain, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Prolactin and pain of endometriosis.Pharmacology & therapeutics · 2023Pooled it
- D1 and D2 neurons in medial nucleus accumbens participate in chronic orofacial pain phenotypes.Pain reports · 2026Article
- Dorsal root ganglion neuromodulation restores accumbal gate to inhibit mechanical allodynia.The journal of headache and pain · 2026Article
- The role of nucleus accumbens dopamine signaling in the development of morphine tolerance in neuropathic pain.The Korean journal of pain · 2026Article
- Adenosine AFrontiers in pharmacology · 2026Article
- Review
- Distinct nucleus accumbens neural pathways underlie separate behavioral features of chronic pain and comorbid depression.The Journal of clinical investigation · 2025Article
- DPsychopharmacology · 2025Article
- Amitriptyline-perphenazine therapy for persistent idiopathic facial pain: translational perspectives from a retrospective study.Journal of anesthesia, analgesia and critical care · 2024Article
- Article
- A common neuronal ensemble in nucleus accumbens regulates pain-like behaviour and sleep.Nature communications · 2023Article
- Pain-related cortico-limbic plasticity and opioid signaling.Neuropharmacology · 2023Review
- Solid-Phase Synthesis of the Bicyclic Peptide OL-CTOP Containing Two Disulfide Bridges, and an Assessment of Its In Vivo μ-Opioid Receptor Antagonism after Nasal Administration.Molecules (Basel, Switzerland) · 2023Article
- Cancer aggravation due to persistent pain signals with the increased expression of pain-related mediators in sensory neurons of tumor-bearing mice.Molecular brain · 2023Article
- Converging circuits between pain and depression: the ventral tegmental area as a therapeutic hub.Frontiers in pharmacology · 2023Review
- Distinct cell populations of ventral tegmental area process motivated behavior.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Review
- VTA-NAc glutaminergic projection involves in the regulation of pain and pain-related anxiety.Frontiers in molecular neuroscience · 2022Article
- Nucleus accumbens shell modulates seizure propagation in a mouse temporal lobe epilepsy model.Frontiers in cell and developmental biology · 2022Article
- Elucidation of the mechanisms of exercise-induced hypoalgesia and pain prolongation due to physical stress and the restriction of movement.Neurobiology of pain (Cambridge, Mass.)Review
- Differential roles of dopamine D1 and D2 receptors in pain modulation: a review.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence suggests that the mesolimbic dopaminergic network plays a role in the modulation of pain. As chronic pain conditions are associated with hypodopaminergic tone in the nucleus accumbens (NAc), we evaluated the effects of increasing signaling at dopamine D1/D2-expressing neurons in the NAc neurons in a model of neuropathic pain induced by partial ligation of sciatic nerve. Bilateral microinjection of either the selective D1-receptor (Gs-coupled) agonist Chloro-APB or the selective D2-receptor (Gi-coupled) agonist quinpirole into the NAc partially reversed nerve injury-induced thermal allodynia. Either optical stimulation of D1-receptor-expressing neurons or optical suppression of D2-receptor-expressing neurons in both the inner and outer substructures of the NAc also transiently, but significantly, restored nerve injury-induced allodynia. Under neuropathic pain-like condition, specific facilitation of terminals of D1-receptor-expressing NAc neurons projecting to the VTA revealed a feedforward-like antinociceptive circuit. Additionally, functional suppression of cholinergic interneurons that negatively and positively control the activity of D1- and D2-receptor-expressing neurons, respectively, also transiently elicited anti-allodynic effects in nerve injured animals. These findings suggest that comprehensive activation of D1-receptor-expressing neurons and integrated suppression of D2-receptor-expressing neurons in the NAc may lead to a significant relief of neuropathic pain.
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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.