ArticlePloS one2014
Altered formalin-induced pain and Fos induction in the periaqueductal grey of preadolescent rats following neonatal LPS exposure.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Fos Protein as a Marker of Neuronal Activity: a Useful Tool in the Study of the Mechanism of Action of Natural Products with Analgesic Activity.Molecular neurobiology · 2018Pooled it
- Changes in the analgesic mechanism of oxytocin can contribute to hyperalgesia in Parkinson's disease model rats.PloS one · 2024Article
- Low-quality protein modulates inflammatory markers and the response to lipopolysaccharide insult: the case of lysine.The British journal of nutrition · 2023Article
- Early life inflammation is associated with spinal cord excitability and nociceptive sensitivity in human infants.Nature communications · 2022Article
- Local injury and systemic infection in infants alter later nociception and pain affect during early life and adulthood.Brain, behavior, & immunity - health · 2020Article
- Neuroimmune modulation of pain across the developmental spectrum.Current opinion in behavioral sciences · 2019Article
- LPS-Induced Systemic Neonatal Inflammation: Blockage of P2X7R by BBG Decreases Mortality on Rat Pups and Oxidative Stress in Hippocampus of Adult Rats.Frontiers in behavioral neuroscience · 2019Article
- Inhibition of AMPA receptor and CaMKII activity in the lateral habenula reduces depressive-like behavior and alcohol intake in rats.Neuropharmacology · 2017Article
- Lifetime Modulation of the Pain SystemFrontiers in immunology · 2017Review
- Early life programming of pain: focus on neuroimmune to endocrine communication.Journal of translational medicine · 2016Review
- Honokiol for the Treatment of Neonatal Pain and Prevention of Consequent Neurobehavioral Disorders.Journal of natural products · 2015Article
- Recruitment of hypothalamic orexin neurons after formalin injections in adult male rats exposed to a neonatal immune challenge.Frontiers in neuroscience · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Animal and human studies have demonstrated that early pain experiences can produce alterations in the nociceptive systems later in life including increased sensitivity to mechanical, thermal, and chemical stimuli. However, less is known about the impact of neonatal immune challenge on future responses to noxious stimuli and the reactivity of neural substrates involved in analgesia. Here we demonstrate that rats exposed to Lipopolysaccharide (LPS; 0.05 mg/kg IP, Salmonella enteritidis) during postnatal day (PND) 3 and 5 displayed enhanced formalin-induced flinching but not licking following formalin injection at PND 22. This LPS-induced hyperalgesia was accompanied by distinct recruitment of supra-spinal regions involved in analgesia as indicated by significantly attenuated Fos-protein induction in the rostral dorsal periaqueductal grey (DPAG) as well as rostral and caudal axes of the ventrolateral PAG (VLPAG). Formalin injections were associated with increased Fos-protein labelling in lateral habenula (LHb) as compared to medial habenula (MHb), however the intensity of this labelling did not differ as a result of neonatal immune challenge. These data highlight the importance of neonatal immune priming in programming inflammatory pain sensitivity later in development and highlight the PAG as a possible mediator of this process.
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