TY - JOUR
T1 - Intracerebroventricular injection of interleukin-6 induces thermal hyperalgesia in rats
AU - Oka, Takakazu
AU - Oka, Kae
AU - Hosoi, Masako
AU - Hori, Tetsuro
N1 - Funding Information:
We thankY . Hirai and Y. Masui,I nstituteo f Cellular TechnologyO, tsukaP harmaceuticaTlo, kushimaJ,a pan, for theirk ind supplyo f IL-lra. We area lsog ratefutlo Dr. B. Quinn,K yushuU niversityf,o r editingt hel anguageo f them anuscripTt.h is work was performetdh roughS pecial CoordinatioFnu ndso f theS ciencea ndT echnologAyg ency of the JapaneseG overnmen(tt o T.H.) andw as also sup-portedin partb y a Grant-in-Aidfo r ScientificR esearchon PriorityA reas' Pain'( No. 0326010t2o T.H,) anda Grant-in-Aid for GeneraSl cientificR esearch(N o. 0645415a3n d 04454144to T.H.) from the Ministry of EducationS, ci-ence,a ndC ultureJ,a pan. This experimenwt as reviewedb y the Committeeo f Ethicso n AnimalE xperimentins theF acultyo f Medicine, KyushuU niversitya ndc arriedo utu ndert hec ontrool f the Guidelinesf or Animal Experimentsin the Faculty of Medicine,K yushuU niversitya ndt he Law (No. 105)a nd Notification(N o. 6) of theJ apaneseg overnment.
PY - 1995/9/18
Y1 - 1995/9/18
N2 - We assessed the effect of interleukin-6 (IL-6) in the brain on nociception by using the hot-plate test in rats. Recombinant human IL-6 (rhIL-6, 30 pg-300 ng) was microinjected into the lateral cerebroventricle (LCV) and the paw-withdrawal latency was then measured for 60 min after injection. RhIL-6 at 300 pg reduced the paw-withdrawal latency at 15 min after injection. Further increase of rhIL-6 doses to 3, 30 and 300 ng resulted in the decreased paw-withdrawal latency at 15 and 30 min. Although the peak responses observed at 3-300 ng did not differ significantly, the time taken for recovery tended to be longer with increasing doses. The rhIL-6 (30 ng)-induced reduction of the paw-withdrawal latency was completely blocked by the co-injection of either Na salicylate (30 ng, LCV) or α-melanocyte stimulating hormone (30 ng, LCV), an anti-cytokine substance. However, it was not affected by the co-injection of IL-1 receptor antagonist (30 ng, LCV) which had been previously shown to be able to block IL-1β-induced hyperalgesia. These findings indicate that IL-6 in the brain induces hyperalgesia by its prostanoids-dependent action in rats. The hyperalgesic action of central IL-6 thus does not appear to depend on the action of IL-1.
AB - We assessed the effect of interleukin-6 (IL-6) in the brain on nociception by using the hot-plate test in rats. Recombinant human IL-6 (rhIL-6, 30 pg-300 ng) was microinjected into the lateral cerebroventricle (LCV) and the paw-withdrawal latency was then measured for 60 min after injection. RhIL-6 at 300 pg reduced the paw-withdrawal latency at 15 min after injection. Further increase of rhIL-6 doses to 3, 30 and 300 ng resulted in the decreased paw-withdrawal latency at 15 and 30 min. Although the peak responses observed at 3-300 ng did not differ significantly, the time taken for recovery tended to be longer with increasing doses. The rhIL-6 (30 ng)-induced reduction of the paw-withdrawal latency was completely blocked by the co-injection of either Na salicylate (30 ng, LCV) or α-melanocyte stimulating hormone (30 ng, LCV), an anti-cytokine substance. However, it was not affected by the co-injection of IL-1 receptor antagonist (30 ng, LCV) which had been previously shown to be able to block IL-1β-induced hyperalgesia. These findings indicate that IL-6 in the brain induces hyperalgesia by its prostanoids-dependent action in rats. The hyperalgesic action of central IL-6 thus does not appear to depend on the action of IL-1.
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U2 - 10.1016/0006-8993(95)00691-I
DO - 10.1016/0006-8993(95)00691-I
M3 - Article
C2 - 8548295
AN - SCOPUS:0029075998
SN - 0006-8993
VL - 692
SP - 123
EP - 128
JO - Brain Research
JF - Brain Research
IS - 1-2
ER -