INTRACEREBROVENTRICULAR INJECTION OF INTERLEUKIN-1-BETA INDUCES HYPERALGESIA IN RATS

INTRACEREBROVENTRICULAR INJECTION OF INTERLEUKIN-1-BETA INDUCES HYPERALGESIA IN RATS
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DOI:
10.1016/0006-8993(93)90060-z
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发表时间:
1993-10-08
期刊:
影响因子:
2.9
通讯作者:
HORI, T
HORI, T
中科院分区:
医学3区
文献类型:
--
作者:
OKA, T;AOU, S;HORI, T

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为了确定脑中的白细胞介素-1 β(IL-1 β)是否可以调节伤害感受,将重组人IL-1 β(rhIL-1 β)(1 μ g/kg至1 μ g/kg)显微注射到大鼠的侧脑室中,并测量在置于热板(50.0+/-0.1 ℃)上后开始舔后爪之前的潜伏期。注射无热原剂量(10 pg/kg ~ 1 ng/kg)的rhIL-1 β可明显缩短小鼠的舔爪潜伏期,100 pg/kg剂量组出现最大反应,注射后5 min开始出现,30 min内达高峰,随后逐渐消退。将rhIL-1 β的量增加到> 1 ng/kg(高达1 μ g/kg)对伤害性阈值没有影响。预先给予IL-1受体拮抗剂(IL-1 ra)或水杨酸钠可完全消除rhIL-1 β诱导的痛觉过敏。α-黑素细胞刺激素(α-MSH)预处理也能抑制rhIL-1 β诱导的痛觉过敏。结果提示,脑内IL-1 β通过受体介导的和对α-MSH敏感的肾上腺素依赖性作用产生痛觉过敏。中枢IL-1的痛觉过敏作用似乎不依赖于CRF系统。
To determine whether interleukin-1beta (IL-1beta) in the brain may modulate nociception, recombinant human IL-1beta (rhIL-1beta) (1 pg/kg to 1 mug/kg) was microinjected into the 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-degrees-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-1beta, 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-1beta to > 1 ng/kg (up to 1 mug/kg) had no effect on the nociceptive threshold. The rhIL-1beta-induced hyperalgesia was completely abolished by pretreatment with an IL-1 receptor antagonist (IL-1ra) or Na salicylate. Similar pretreatment with alpha-melanocyte-stimulating hormone (alpha-MSH) also inhibited the rhIL-1beta-induced hyperalgesia. However, pretreatment with alpha-helical corticotropin-releasing factor (CRF)9-41 failed to affect it. The results suggest that IL-1beta in the brain produces hyperalgesia by its receptor-mediated and prostaglandin-dependent action which is sensitive to alpha-MSH. The hyperalgesic action of central IL-1 does not appear to depend on the CRF system.