ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Plasticity in the Link between Pain-Transmitting and Pain-Modulating Systems in Acute and Persistent Inflammation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Effects of photobiomodulation therapy on upper limb lymphedema secondary to breast cancer: a systematic review and meta-analysis.Frontiers in oncology · 2026Review
- The relationship between neighborhood disadvantage and markers of chronic pain risk: Findings from the Oklahoma Study of Native American Pain Risk (OK-SNAP).The journal of pain · 2025Article
- Neural Circuit Connections and Functions of Locus Coeruleus-Norepinephrine System.International journal of molecular sciences · 2025Review
- HSPA1A Can Alleviate CFA-Induced Inflammatory Pain by Modulating Macrophages.International journal of molecular sciences · 2025Article
- Article
- The 'in's and out's' of descending pain modulation from the rostral ventromedial medulla.Trends in neurosciences · 2024Review
- The parabrachial to central amygdala pathway is critical to injury-induced pain sensitization in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Repeated closed-head mild traumatic brain injury-induced inflammation is associated with nociceptive sensitization.Journal of neuroinflammation · 2023Article
- The locus coeruleus input to the rostral ventromedial medulla mediates stress-induced colorectal visceral pain.Acta neuropathologica communications · 2023Article
- The parabrachial to central amygdala circuit is a key mediator of injury-induced pain sensitization.bioRxiv : the preprint server for biology · 2023Article
- Molecular identification of bulbospinal ON neurons by GPER, which drives pain and morphine tolerance.The Journal of clinical investigation · 2023Article
- Bulbospinal nociceptive ON and OFF cells related neural circuits and transmitters.Frontiers in pharmacology · 2023Review
- From Low-Grade Inflammation in Osteoarthritis to Neuropsychiatric Sequelae: A Narrative Review.International journal of molecular sciences · 2022Review
- A nigro-subthalamo-parabrachial pathway modulates pain-like behaviors.Nature communications · 2022Article
- Article
- Sex differences in pain along the neuraxis.Neuropharmacology · 2022Review
- Review
- NMDARs mediate peripheral and central sensitization contributing to chronic orofacial pain.Frontiers in cellular neuroscience · 2022Review
- Shifting the Balance: How Top-Down and Bottom-Up Input Modulate PainFrontiers in pain research (Lausanne, Switzerland) · 2022Review
- Brainstem Mechanisms of Pain Modulation: A within-Subjects 7T fMRI Study of Placebo Analgesic and Nocebo Hyperalgesic Responses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
There is strong evidence that spinoparabrachial neurons in the superficial dorsal horn contribute to persistent pain states, and that the lateral parabrachial complex (PB) conveys relevant nociceptive information to higher structures. The role of PB itself in hyperalgesia and how it recruits descending facilitation has nevertheless received significantly less attention. The current study is a first step toward delineating the functional dynamics of PB and its link to descending control in acute and persistent inflammatory pain. In lightly anesthetized rats, we recorded behavioral withdrawal evoked by mechanical stimulation of the hindpaw and, simultaneously, the activity of identified pain-modulating neurons, "ON-cells" and "OFF-cells," in the rostral ventromedial medulla (RVM). This was done before and after the inactivation of PB, contralateral or ipsilateral to an inflamed paw [1 h, 1 d, or 5-6 d after intraplantar injection of Complete Freund's Adjuvant (CFA)]. The inactivation of contralateral, but not ipsilateral, PB interfered with nociceptive input to RVM under basal conditions, as well as in acute inflammation. By contrast, blocking ipsilateral, but not contralateral, PB in established inflammation interfered with behavioral hyperalgesia and ON-cell and OFF-cell responses. The lesioning of contralateral PB before CFA injection prevented this recruitment of ipsilateral PB in persistent inflammation. These experiments show that contralateral PB is required to initiate hyperalgesia, which is then maintained by ipsilateral PB, most likely in both cases via the engagement of pain-modulating neurons of the RVM.
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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.