Central interleukin-1β enhances splenic sympathetic nerve activity in rats

Tomoyasu Ichijo, Toshihiko Katafuchi, Tetsuro Hori

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64 Citations (Scopus)


The central administration of immune cytokines such as interleukin-1 (IL-1) and interferon-α (IFN-α) results in the suppression of peripheral cellular immunity, which depends, at least partly, on the sympathetic nervous activity. An intrathird cerebroventricular (I3V) infusion of recombinant human IL-1β (rhIL-1β) (1-5 ng/rat) elicited a dosedependent increase in the electrical activity of the splenic sympathetic nerve in urethane and α-chloralose anesthetized rats. The effect of rhIL-1β (1 ng/rat) was completely blocked by pretreatment with an IL-1 receptor antagonist (1 μg/rat, I3V 10 min before rhIL-1β), sodium salicylate (1 μg/rat), or α-melanocyte stimulating hormone (α-MSH) (400 ng/rat). Furthermore, an antagonist of corticotropin-releasing factor (CRF), α-helical CRF9.41 (2 μg/rat), completely abolished the rhIL-1β-induced increase in the splenic nerve activity, although an I3V infusion of CRF (1 μg/rat) excited it. These results suggest that IL-1β in the brain activates splenic sympathetic activity by its receptor-mediated and prostaglandin-dependent action that is sensitive to α-MSH, depending on CRF system. Our findings, together with the previous results, suggest that the splenic sympathetic nerve represents one of the communication channels from the brain to the immune system.

Original languageEnglish
Pages (from-to)547-553
Number of pages7
JournalBrain Research Bulletin
Issue number6
Publication statusPublished - 1994

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)


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