TY - JOUR
T1 - Intracerebroventricular injection of interleukin-1β induces hyperalgesia in rats
AU - Oka, Takakazu
AU - Aou, Shuji
AU - Hori, Tetsuro
N1 - Funding Information:
Acknowledgements. We thank Y. Hirai and Y. Masui, Institute of Cellular Technology, Otsuka Pharmaceutical, Tokushima, Japan, for their kind supply of rhlL-1/3 and IL-lra. We are grateful to B.C. Quin, Kyushu University, for reading the manuscript. This work was supported in part by Grant-in-Aid for Scientific Research on Priority Areas "Pain" 03260102 (to T. Hori) and Grant-in-Aid for General Scientific Research 04454144 (to T. Hori) from the Ministry of Education, Science and Culture, Japan.
PY - 1993/10/8
Y1 - 1993/10/8
N2 - To determine whether interleukin-1β (IL-1β) in the brain may modulate nociception, recombinant human IL-1β (rhIL-1β) (1pg/kg to 1 μg/kg) was microinjected into lateral cerebral ventricle of rats and the latency before initiating the licking of their hindpaws after being placed on a hot plate (50.0 ± 0.1°C) was measured. A significant reduction of the paw-lick latency was observed after injections of nonpyrogenic doses (10 pg/kg to 1 ng/kg) of rhIL-1β, showing a maximal response at a dose of 100 pg/kg which began to appear 5 min after injection, reached a peak within 30 min and then gradually subsided. An increase in the amount of rhIL-1β to > 1 ng/kg (up to 1 μg/kg had no effect on the nociceptive threshold. The rhIL-1β-induced hyperalgesia was completely abolished by pretreatment with an IL-1 receptor antagonist (IL-1ra) or Na salicylate. Similar pretreatment with α-melanocyte-stimulating hormone (α-MSH) also inhibited the rhIL-1β-induced hyperalgesia. However, pretreatment with α-helical corticotropin-releasing factor (CRF)9-41 failed to affect it. The results suggest that IL-1β in the brain produces hyperalgesia by its receptor-mediated and prostaglandin-dependent action which is sensitive to α-MSH. The hyperalgesic action of central IL-1 does not appear to depende on the CRF system.
AB - To determine whether interleukin-1β (IL-1β) in the brain may modulate nociception, recombinant human IL-1β (rhIL-1β) (1pg/kg to 1 μg/kg) was microinjected into lateral cerebral ventricle of rats and the latency before initiating the licking of their hindpaws after being placed on a hot plate (50.0 ± 0.1°C) was measured. A significant reduction of the paw-lick latency was observed after injections of nonpyrogenic doses (10 pg/kg to 1 ng/kg) of rhIL-1β, showing a maximal response at a dose of 100 pg/kg which began to appear 5 min after injection, reached a peak within 30 min and then gradually subsided. An increase in the amount of rhIL-1β to > 1 ng/kg (up to 1 μg/kg had no effect on the nociceptive threshold. The rhIL-1β-induced hyperalgesia was completely abolished by pretreatment with an IL-1 receptor antagonist (IL-1ra) or Na salicylate. Similar pretreatment with α-melanocyte-stimulating hormone (α-MSH) also inhibited the rhIL-1β-induced hyperalgesia. However, pretreatment with α-helical corticotropin-releasing factor (CRF)9-41 failed to affect it. The results suggest that IL-1β in the brain produces hyperalgesia by its receptor-mediated and prostaglandin-dependent action which is sensitive to α-MSH. The hyperalgesic action of central IL-1 does not appear to depende on the CRF system.
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U2 - 10.1016/0006-8993(93)90060-Z
DO - 10.1016/0006-8993(93)90060-Z
M3 - Article
C2 - 8252417
AN - SCOPUS:0027304730
SN - 0006-8993
VL - 624
SP - 61
EP - 68
JO - Molecular Brain Research
JF - Molecular Brain Research
IS - 1-2
ER -