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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: UNLABELLED. Meshes: Animals, Carrageenan, Chronic Disease, Dinoprostone, Disease Models, Animal, Enzyme Activation, Hyperalgesia, Injections, Intramuscular, Injections, Spinal, Male, Muscle, Skeletal, Myositis, Neuronal Plasticity, Neurons, Afferent, Nociceptors, Oligodeoxyribonucleotides, Antisense, Pain, Protein Kinase C-epsilon, Rats, Rats, Sprague-Dawley.
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Does muscle inflammation induce a protein kinase Cepsilon-dependent chronic-latent muscle pain? Context: Skeletal muscle injuries can induce chronic pain, but the underlying mechanism is unknown. One possible cause has been suggested to be an increased sensitivity to inflammatory mediators. We demonstrate that self-limited inflammatory hyperalgesia induced by intramuscular carrageenan (lasting approximately 5 days) results in a state of chronic-latent hyperalgesia, revealed by injection of prostaglandin E(2) (PGE(2)) 10 days after carrageenan at the same site. In carrageenan-pretreated muscle, PGE(2) produced hyperalgesia that was unattenuated even 14 days after injection, markedly longer than the 4-hour hyperalgesia induced by PGE(2) in naive rats. This chronic-latent hyperalgesia was reversed as well as prevented by spinal intrathecal injection of oligodeoxynucleotide antisense to protein kinase Cepsilon, a second messenger implicated in long-lasting plasticity in cutaneous nociceptors.
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We describe a novel experimental model for chronic muscle pain, produced by mild acute muscle inflammation, that has clinical significance since it has the potential to reveal cellular processes by which acute inflammation or muscle trauma underlies chronic muscle pain. Final Decision: yes