Differential Modulatory Effects of Cholera Toxin and Pertussis Toxin on Pain Behavior Induced by TNF-${\alpha}$, Interleukin-1${\beta}$ and Interferon-${\gamma}$ Injected Intrathecally

  • Kwon, Min-Soo (Department of Pharmacology, College of Medicine, and Institute of Natural Medicine, Hallym University) ;
  • Shim, Eon-Jeong (Department of Pharmacology, College of Medicine, and Institute of Natural Medicine, Hallym University) ;
  • Seo, Young-Jun (Department of Pharmacology, College of Medicine, and Institute of Natural Medicine, Hallym University) ;
  • Choi, Seong-Soo (Department of Pharmacology, College of Medicine, and Institute of Natural Medicine, Hallym University) ;
  • Lee, Jin-Young (Department of Pharmacology, College of Medicine, and Institute of Natural Medicine, Hallym University) ;
  • Lee, Han-Kyu (Department of Pharmacology, College of Medicine, and Institute of Natural Medicine, Hallym University) ;
  • Suh, Hong-Won (Department of Pharmacology, College of Medicine, and Institute of Natural Medicine, Hallym University)
  • Published : 2005.01.01

Abstract

The present study was designed to characterize the possible roles of spinally located cholera toxin (CTX)- and pertussis toxin (PTX)-sensitive G-proteins in pro- inflammatory cy tokine induced pain behaviors. Intrathecal injection of tumor necrosis factor-a (TNF-${\alpha}$; 100 pg), interleukin-1${\beta}$ (IL-1${\beta}$ 100 pg) and interferon-${\gamma}$ (INF-${\gamma}$; 100 pg) showed pain behavior. Intrathecal pretreatment with CTX (0.05, 0.1 and 0.5 mg) attenuated pain behavior induced by TNF-${\alpha}$ and INF-${\gamma}$ administered intrathecally. But intrathecal pretreatment with CTX (0.05, 0.1 and 0.5${\mu}g$) did not attenuate pain behavior induced by IL-1${\beta}$. On the other hand, intrathecal pretreatment with PTX further increased the pain behavior induced by TNF-${\alpha}$ and IL-1${\beta}$ administered intrathecally, especially at the dose of 0.5 ${\mu}g$. But intrathecal pretreatment with PTX did not affect pain behavior induced by INF-${\gamma}$. Our results suggest that, at the spinal cord level, CTX- and PTX-sensitive G-proteins appear to play important roles in modulating pain behavior induced by pro-inflammatory cytokines administered spinally. Furthermore, TNF-${\alpha}$, IL-1${\beta}$ arid INF-${\gamma}$ administered spinally appear to produce pain behavior by different mechanisms.

Keywords

References

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