Abstract：
:Interleukin-1 is known to exert pleiotropic effects in host defence mechanisms and in inflammation. Chronic pain, inflammation and interleukin-1 beta enhance the production of substance P. Recently, axonal transport of opiate receptors was found to increase in rat sciatic nerves in the model of Freund's adjuvant-induced arthritis. Here we show that a single intraplantar injection of interleukin-1 beta is able to enhance the axonal transport of mu and kappa opiate receptors and substance P. Indeed, their accumulation was markedly increased in the proximal part of ligated sciatic nerves, but only in the paw injected with interleukin-1. The time course revealed a delayed onset and, more importantly, a long-term increase lasting at least six days, which is in contrast with the short-term pyrogenic effect of interleukin-1. Pretreatment of rats with capsaicin or administration of dexamethasone completely prevented the interleukin-1 beta effect. The present results suggest that interleukin-1 beta may serve as a mediator to sensitize nociceptors in chronic inflammation and possibly in hyperalgesia through long-term changes in neuronal plasticity.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Jeanjean AP,Moussaoui SM,Maloteaux JM,Laduron PMdoi
10.1016/0306-4522(95)00106-ssubject
Has Abstractpub_date
1995-09-01 00:00:00pages
151-7issue
1eissn
0306-4522issn
1873-7544pii
030645229500106Sjournal_volume
68pub_type
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