Intracerebroventricular injection of tumor necrosis factor-α induces thermal hyperalgesia in rats

Takakazu Oka, Yoshiyuki Wakugawa, Masako Hosoi, Kae Oka, Tetsuro Hori

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

To investigate the role of tumor necrosis factor-α(TNF-α) in the brain in nociception, we injected recombinant human TNF-α(rhTNF-α; 1 pg-10 ng/rat) into the lateral cerebroventricle (LCV) in rats and observed the changes in paw withdrawal latency to radiant heat by using the plantar test for 90 min after injection. LCV injections of TNF-αat doses of 10 pg, 100 pg and 1 ng reduced paw withdrawal latency, showing a maximal response at a dose of 10 pg which peaked 60 min after injection. TNF-αat doses of 1 pg and 10 ng had no effect on nociception during the test period. The TNF-α(10 pg)-induced reduction in paw withdrawal latency was blocked by simultaneous injection of diclofenac (1 ng), a cyclooxygenase inhibitor, or interleukin-1 receptor antagonist (IL-1ra, 10 ng). LCV injection of neither diclofenac (1 ng) nor IL-1ra (10 ng) had any effect on nociception by itself. The results suggest that TNF-αin the brain induces thermal hyperalgesia and that the brain TNF-α-induced hyperalgesia is mediated by the central action of interleukin-1 and activation of the cyclooxygenase pathway of the arachidonate.

Original languageEnglish
Pages (from-to)135-140
Number of pages6
JournalNeuroImmunoModulation
Volume3
Issue number2-3
DOIs
Publication statusPublished - Jan 1 1996

Fingerprint

Hyperalgesia
Tumor Necrosis Factor-alpha
Injections
Interleukin 1 Receptor Antagonist Protein
Nociception
Diclofenac
Interleukin-10
Brain
Interleukin-1 Receptors
Cyclooxygenase Inhibitors
Pain Measurement
Prostaglandin-Endoperoxide Synthases
Interleukin-1
Hot Temperature

All Science Journal Classification (ASJC) codes

  • Immunology
  • Endocrinology
  • Neurology
  • Endocrine and Autonomic Systems

Cite this

Intracerebroventricular injection of tumor necrosis factor-α induces thermal hyperalgesia in rats. / Oka, Takakazu; Wakugawa, Yoshiyuki; Hosoi, Masako; Oka, Kae; Hori, Tetsuro.

In: NeuroImmunoModulation, Vol. 3, No. 2-3, 01.01.1996, p. 135-140.

Research output: Contribution to journalArticle

Oka, Takakazu ; Wakugawa, Yoshiyuki ; Hosoi, Masako ; Oka, Kae ; Hori, Tetsuro. / Intracerebroventricular injection of tumor necrosis factor-α induces thermal hyperalgesia in rats. In: NeuroImmunoModulation. 1996 ; Vol. 3, No. 2-3. pp. 135-140.
@article{edff3892b74d4c978ac25efdebb1942d,
title = "Intracerebroventricular injection of tumor necrosis factor-α induces thermal hyperalgesia in rats",
abstract = "To investigate the role of tumor necrosis factor-α(TNF-α) in the brain in nociception, we injected recombinant human TNF-α(rhTNF-α; 1 pg-10 ng/rat) into the lateral cerebroventricle (LCV) in rats and observed the changes in paw withdrawal latency to radiant heat by using the plantar test for 90 min after injection. LCV injections of TNF-αat doses of 10 pg, 100 pg and 1 ng reduced paw withdrawal latency, showing a maximal response at a dose of 10 pg which peaked 60 min after injection. TNF-αat doses of 1 pg and 10 ng had no effect on nociception during the test period. The TNF-α(10 pg)-induced reduction in paw withdrawal latency was blocked by simultaneous injection of diclofenac (1 ng), a cyclooxygenase inhibitor, or interleukin-1 receptor antagonist (IL-1ra, 10 ng). LCV injection of neither diclofenac (1 ng) nor IL-1ra (10 ng) had any effect on nociception by itself. The results suggest that TNF-αin the brain induces thermal hyperalgesia and that the brain TNF-α-induced hyperalgesia is mediated by the central action of interleukin-1 and activation of the cyclooxygenase pathway of the arachidonate.",
author = "Takakazu Oka and Yoshiyuki Wakugawa and Masako Hosoi and Kae Oka and Tetsuro Hori",
year = "1996",
month = "1",
day = "1",
doi = "10.1159/000097238",
language = "English",
volume = "3",
pages = "135--140",
journal = "NeuroImmunoModulation",
issn = "1021-7401",
publisher = "S. Karger AG",
number = "2-3",

}

TY - JOUR

T1 - Intracerebroventricular injection of tumor necrosis factor-α induces thermal hyperalgesia in rats

AU - Oka, Takakazu

AU - Wakugawa, Yoshiyuki

AU - Hosoi, Masako

AU - Oka, Kae

AU - Hori, Tetsuro

PY - 1996/1/1

Y1 - 1996/1/1

N2 - To investigate the role of tumor necrosis factor-α(TNF-α) in the brain in nociception, we injected recombinant human TNF-α(rhTNF-α; 1 pg-10 ng/rat) into the lateral cerebroventricle (LCV) in rats and observed the changes in paw withdrawal latency to radiant heat by using the plantar test for 90 min after injection. LCV injections of TNF-αat doses of 10 pg, 100 pg and 1 ng reduced paw withdrawal latency, showing a maximal response at a dose of 10 pg which peaked 60 min after injection. TNF-αat doses of 1 pg and 10 ng had no effect on nociception during the test period. The TNF-α(10 pg)-induced reduction in paw withdrawal latency was blocked by simultaneous injection of diclofenac (1 ng), a cyclooxygenase inhibitor, or interleukin-1 receptor antagonist (IL-1ra, 10 ng). LCV injection of neither diclofenac (1 ng) nor IL-1ra (10 ng) had any effect on nociception by itself. The results suggest that TNF-αin the brain induces thermal hyperalgesia and that the brain TNF-α-induced hyperalgesia is mediated by the central action of interleukin-1 and activation of the cyclooxygenase pathway of the arachidonate.

AB - To investigate the role of tumor necrosis factor-α(TNF-α) in the brain in nociception, we injected recombinant human TNF-α(rhTNF-α; 1 pg-10 ng/rat) into the lateral cerebroventricle (LCV) in rats and observed the changes in paw withdrawal latency to radiant heat by using the plantar test for 90 min after injection. LCV injections of TNF-αat doses of 10 pg, 100 pg and 1 ng reduced paw withdrawal latency, showing a maximal response at a dose of 10 pg which peaked 60 min after injection. TNF-αat doses of 1 pg and 10 ng had no effect on nociception during the test period. The TNF-α(10 pg)-induced reduction in paw withdrawal latency was blocked by simultaneous injection of diclofenac (1 ng), a cyclooxygenase inhibitor, or interleukin-1 receptor antagonist (IL-1ra, 10 ng). LCV injection of neither diclofenac (1 ng) nor IL-1ra (10 ng) had any effect on nociception by itself. The results suggest that TNF-αin the brain induces thermal hyperalgesia and that the brain TNF-α-induced hyperalgesia is mediated by the central action of interleukin-1 and activation of the cyclooxygenase pathway of the arachidonate.

UR - http://www.scopus.com/inward/record.url?scp=0029845521&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029845521&partnerID=8YFLogxK

U2 - 10.1159/000097238

DO - 10.1159/000097238

M3 - Article

C2 - 8945729

AN - SCOPUS:0029845521

VL - 3

SP - 135

EP - 140

JO - NeuroImmunoModulation

JF - NeuroImmunoModulation

SN - 1021-7401

IS - 2-3

ER -