ArticleFrontiers in immunology2016
Peripheral and Central Neuroinflammatory Changes and Pain Behaviors in an Animal Model of Multiple Sclerosis.
Article in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Protection From Demyelination by the Novel Adenosine Dual AJournal of cellular and molecular medicine · 2025Article
- Grimace scale assessment duringFrontiers in veterinary science · 2023Article
- Sex Differences in the Behavioural Aspects of the Cuprizone-Induced Demyelination Model in Mice.Brain sciences · 2022Article
- Involvement of TLR2-TLR4, NLRP3, and IL-17 in pain induced by a novel Sprague-Dawley rat model of experimental autoimmune encephalomyelitis.Frontiers in pain research (Lausanne, Switzerland) · 2022Article
- Crotalphine Attenuates Pain and Neuroinflammation Induced by Experimental Autoimmune Encephalomyelitis in Mice.Toxins · 2021Article
- Interleukin-6: evolving role in the management of neuropathic pain in neuroimmunological disorders.Inflammation and regeneration · 2021Review
- Periorbital Nociception in a Progressive Multiple Sclerosis Mouse Model Is Dependent on TRPA1 Channel Activation.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Methods Used and Application of the Mouse Grimace Scale in Biomedical Research 10 Years on: A Scoping Review.Animals : an open access journal from MDPI · 2021Article
- Toll-like receptor 2 and 4 antagonism for the treatment of experimental autoimmune encephalomyelitis (EAE)-related pain.Brain, behavior, and immunity · 2021Article
- Neuropathic Pain in Multiple Sclerosis and Its Animal Models: Focus on Mechanisms, Knowledge Gaps and Future Directions.Frontiers in neurology · 2021Review
- TNFα in MS and Its Animal Models: Implications for Chronic Pain in the Disease.Frontiers in neurology · 2021Review
- The Utility of Grimace Scales for Practical Pain Assessment in Laboratory Animals.Animals : an open access journal from MDPI · 2020Review
- Reliability of the Mouse Grimace Scale in C57BL/6JRj Mice.Animals : an open access journal from MDPI · 2020Article
- Inflammation and Oxidative Stress in Multiple Sclerosis: Consequences for Therapy Development.Oxidative medicine and cellular longevity · 2020Review
- Pathological pain processing in mouse models of multiple sclerosis and spinal cord injury: contribution of plasma membrane calcium ATPase 2 (PMCA2).Journal of neuroinflammation · 2019Article
- Exogenous activation of tumor necrosis factor receptor 2 promotes recovery from sensory and motor disease in a model of multiple sclerosis.Brain, behavior, and immunity · 2019Article
- Article
- Regulatory T Cells and Their Derived Cytokine, Interleukin-35, Reduce Pain in Experimental Autoimmune Encephalomyelitis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Welfare and Scientific Considerations of Tattooing and Ear Tagging for Mouse Identification.Journal of the American Association for Laboratory Animal Science : JAALAS · 2019Article
- Anti-IL-6 Receptor Antibody Inhibits Spontaneous Pain at the Pre-onset of Experimental Autoimmune Encephalomyelitis in Mice.Frontiers in neurology · 2019Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pain is a widespread and debilitating symptom of multiple sclerosis (MS), a chronic inflammatory demyelinating disease of the central nervous system. Although central neuroinflammation and demyelination have been implicated in MS-related pain, the contribution of peripheral and central mechanisms during different phases of the disease remains unclear. In this study, we used the animal model experimental autoimmune encephalomyelitis (EAE) to examine both stimulus-evoked and spontaneous pain behaviors, and neuroinflammatory changes, over the course of chronic disease. We found that mechanical allodynia of the hind paw preceded the onset of clinical EAE but was unmeasurable at clinical peak. This mechanical hypersensitivity coincided with increased microglial activation confined to the dorsal horn of the spinal cord. The development of facial mechanical allodynia also emerged in preclinical EAE, persisted at the clinical peak, and corresponded with pathology of the peripheral trigeminal afferent pathway. This included T cell infiltration, which arose prior to overt central lesion formation and specific damage to myelinated neurons during the clinical peak. Measurement of spontaneous pain using the mouse grimace scale, a facial expression-based coding system, showed increased facial grimacing in mice with EAE during clinical disease. This was associated with multiple peripheral and central neuroinflammatory changes including a decrease in myelinating oligodendrocytes, increased T cell infiltration, and macrophage/microglia and astrocyte activation. Overall, these findings suggest that different pathological mechanisms may underlie stimulus-evoked and spontaneous pain in EAE, and that these behaviors predominate in unique stages of the disease.
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