作者: Richard T. Ambron , Maryjane Farr , Jenny Mathews , De-Fen Zhu
DOI: 10.1101/LM.6.3.331
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摘要: Nerve injury, tissue damage, and inflammation all cause hyperalgesia. A factor contributing to this increased sensitivity is a long-term (>24 hr) hyperexcitability (LTH) in the sensory neurons that mediate responses. Using cluster of nociceptive Aplysia californica as model, we are examining how induces LTH. general inflammatory response was induced by inserting gauze pad into animal Within 4 days, enmeshed an amorphous material contains hemocytes, which comprise cellular immune system. Concurrently, LTH appears both ipsilateral contralateral neurons. The manifest action potential discharge normalized stimulus. Immunocytochemistry revealed hemocytes have antigens recognized antibodies TGFbeta1, IL-6, 5HT. When localized elicited on nerve, containing TGFbeta1 antigen were present near axons within nerve those IL-6 surface. Western blots or had foreign body response, contained 28-kD polypeptide anti-TGFbeta1 antibody. Exposure nervous system recombinant human firing decrease threshold. also caused activation protein kinase C (PKC) but did not affect activated after injury. Our findings, conjunction with previous results, indicate TGFbeta1-homolog can modulate activity respond noxious stimuli. This could contribute interactions between systems via regulation PKC.