Vagal afferent input from the acid-challenged rat stomach to the brainstem:: Enhancement by interleukin-1β
Vagal afferent input from the acid-challenged rat stomach to the brainstem:: Enhancement by interleukin-1β
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DOI：
10.1016/j.neuroscience.2004.07.040
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发表时间：
2004-01-01
期刊：
影响因子：
3.3
通讯作者：
Lippe, IT
中科院分区：
文献类型：
--
作者：
Holzer, P;Danzer, M;Lippe, IT
胃粘膜暴露于反向扩散浓度的HCI （0.25 M, pH 0.51）刺激迷走神经传入脑干。在这里，我们研究了用促炎细胞因子白介素-1 β和肿瘤坏死因子- α预处理大鼠是否会导致迷走神经传入通路对HCI的敏感化。大鼠在灌胃HCI (0.25 M, 1 m1/100 g) 24、48和96 h前分别用白细胞介素-1 β、肿瘤坏死因子- α（10杯/kg）或其载体（无菌生理盐水）进行ig预处理。HCI刺激2 h后，用c-Fos免疫组化方法观察孤束核神经元的激活情况。单独给药白细胞介素-1 β和肿瘤坏死因子- α可诱导脑干c-Fos表达，24 h后这种作用消失。此时，HCI对孤立束核c-Fos表达的影响通过白细胞介素-1 β和肿瘤坏死因子- α预处理显著增强。白细胞介素-1 β的增敏作用持续48小时以上，并被白细胞介素-1受体拮抗剂anakinra阻止。脑内给予白细胞介素-1 β和肿瘤坏死因子- α (100 ng)未能增强hci诱发的脑干c-Fos的表达。这些结果表明，外周给药促炎细胞因子白细胞介素-1 β和肿瘤坏死因子α可诱导迷走神经传入通路对胃HCI攻击的长时间敏化。这种作用似乎是由迷走神经传入的外周作用引起的，可能与胃化学感觉有关。2004年由Elsevier Ltd代表IBRO出版。
Exposure of the gastric mucosa to back-diffusing concentrations of HCI (0.25 M, pH 0.51) stimulates vagal afferent input to the brainstem. Here we have examined whether pretreatment of rats with the proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha causes sensitization of vagal afferent pathways to HCI. Rats were pretreated i.p. with interleukin-1beta, tumor necrosis factor-alpha (10 mug/kg) or their vehicle (sterile saline) 24, 48 and 96 h before intragastric administration of HCI (0.25 M, 1 m1/100 g). Activation of neurons in the nucleus tractus solitarii was visualized by c-Fos immunohistochemistry 2 h after the HCI challenge. I.p. administration of interleukin-1beta and tumor necrosis factor-alpha alone induced c-Fos in the brainstem, an effect that was gone after 24 h. At this time, however, the effect of HCI to cause expression of c-Fos in the nucleus tractus solitarii was significantly enhanced by pretreatment with interleukin-1beta and tumor necrosis factor-alpha. The sensitizing effect of i.p.-administered interleukin-1beta was sustained for more than 48 h and prevented by the interleukin-1 receptor antagonist anakinra. Intracisternal administration of interleukin-1beta and tumor necrosis factor-alpha (100 ng) failed to amplify the HCI-evoked expression of c-Fos in the brainstem.These results show that peripheral administration of the proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha induces prolonged sensitization of vagal afferent pathways to gastric HCI challenge. This effect seems to arise from a peripheral action on vagal afferents and may be of relevance to gastric chemonociception. 2004 Published by Elsevier Ltd on behalf of IBRO.