ArticleMolecular pain2012
Up-regulation of platelet-activating factor synthases and its receptor in spinal cord contribute to development of neuropathic pain following peripheral nerve injury.
Article in Molecular pain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Different genes may be involved in distal and local sensitization: A genome-wide gene-based association study and meta-analysis.European journal of pain (London, England) · 2022Pooled it
- Sex- and APOE Genotype-Dependent Pain Susceptibility and Alzheimer's Risk Mediated by the Lipid Metabolism Enzyme LPCAT2.Aging cell · 2025Article
- Neuroinflammation Involving Endothelin-1 and Platelet-Activating Factor Receptors Contributes To Self-Injurious Behaviors Induced by Bay k-8644 in Adolescent Mice.Neurochemical research · 2025Article
- Macrophage/microglia-producing transient increase of platelet-activating factor is involved in neuropathic pain.iScience · 2024Article
- Role of Neurons and Glia Cells in Wound Healing as a Novel Perspective Considering Platelet as a Conventional Player.Molecular neurobiology · 2022Review
- Role of Microglia and Astrocytes in Spinal Cord Injury Induced Neuropathic Pain.Annals of neurosciences · 2021Review
- Current Understanding of Platelet-Activating Factor Signaling in Central Nervous System Diseases.Molecular neurobiology · 2017Review
- Relief from neuropathic pain by blocking of the platelet-activating factor-pain loop.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Platelet Activating Factor Enhances Synaptic Vesicle Exocytosis Via PKC, Elevated Intracellular Calcium, and Modulation of Synapsin 1 Dynamics and Phosphorylation.Frontiers in cellular neuroscience · 2015Article
- Transactivation of epidermal growth factor receptor through platelet-activating factor/receptor in ovarian cancer cells.Journal of experimental & clinical cancer research : CR · 2014Article
- Diversity and function of membrane glycerophospholipids generated by the remodeling pathway in mammalian cells.Journal of lipid research · 2014Review
- Spinal cord stimulation reduces mechanical hyperalgesia and glial cell activation in animals with neuropathic pain.Anesthesia and analgesia · 2014Article
- Palliation of bone cancer pain by antagonists of platelet-activating factor receptors.PloS one · 2014Article
- Reverse transcription quantitative real-time polymerase chain reaction reference genes in the spared nerve injury model of neuropathic pain: validation and literature search.BMC research notes · 2013Article
- The role of PAF/PAFR signaling in zymosan-induced articular inflammatory hyperalgesia.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPlatelet-activating factor (PAF; 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is a lipid mediator derived from cell membrane. It has been reported that PAF is involved in various pathological conditions, such as spinal cord injury, multiple sclerosis, neuropathic pain and intrathecal administration of PAF leads to tactile allodynia. However, the expression of PAF synthases and its receptor in the spinal cord following peripheral nerve injury is unknown.
methodsUsing the rat spared nerve injury (SNI) model, we investigated the expression of PAF synthases (LPCAT1 and 2) and PAF receptor (PAFr) mRNAs in the spinal cord. Reverse transcription polymerase chain reaction (RT-PCR) and double-labeling analysis of in situ hybridization histochemistry (ISHH) with immunohistochemistry (IHC) were employed for the analyses. Pain behaviors were also examined with PAFr antagonist (WEB2086).
resultsRT-PCR showed that LPCAT2 mRNA was increased in the ipsilateral spinal cord after injury, but not LPCAT1 mRNA. Double-labeling of ISHH with IHC revealed that LPCAT1 and 2 mRNAs were constitutively expressed by a subset of neurons, and LPCAT2 mRNA was increased in spinal microglia after nerve injury. RT-PCR showed that PAFr mRNA was dramatically increased in the ipsilateral spinal cord after nerve injury. Double-labeling analysis of ISHH with IHC revealed that after injury PAFr mRNA was predominantly colocalized with microglia in the spinal cord. Continuous intrathecal administration of the PAFr antagonist suppressed mechanical allodynia following peripheral nerve injury. Delayed administration of a PAFr antagonist did not reverse the mechanical allodynia.
conclusionsOur data show the histological localization of PAF synthases and its receptor in the spinal cord following peripheral nerve injury, and suggest that PAF/PAFr signaling in the spinal cord acts in an autocrine or paracrine manner among the activated microglia and neurons, thus contributing to development of neuropathic pain.
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