Evidence that the bed nucleus of the stria terminalis contributes to the modulation of hypophysiotropic corticotropin-releasing factor cell responses to systemic interleukin-1β
Evidence that the bed nucleus of the stria terminalis contributes to the modulation of hypophysiotropic corticotropin-releasing factor cell responses to systemic interleukin-1β
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DOI：
10.1002/cne.10918
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发表时间：
2003-12-08
影响因子：
2.5
通讯作者：
Day, TA
中科院分区：
文献类型：
--
作者：
Crane, JW;Buller, KM;Day, TA
全身感染会激活下丘脑-垂体-肾上腺 (HPA) 轴，而脑干儿茶酚胺细胞已被证明有助于这种反应。然而，最近的研究也表明中央杏仁核（CeA）发挥着重要作用。由于 CeA 和 HPA 轴下丘脑尖部之间的直接连接很少，本研究调查了终纹床核 (BNST) 是否可能充当它们之间的中继。这是通过使用急性全身感染的动物模型来完成的，该模型涉及血管内递送促炎细胞因子白细胞介素-1β（IL-1β，1 杯/千克）。包围腹侧 BNST 的单侧鹅膏蕈酸损伤显着降低了 IL-1β 诱导的下丘脑室旁核 (PVN) 促肾上腺皮质激素释放因子 (CRF) 细胞 Fos 免疫反应性的增加以及促肾上腺皮质激素 (ACTH) 分泌的相应增加。类似的损伤对 CRF 细胞对身体约束的反应没有影响，这表明 BNST 损伤的影响并不是由于对应激反应的非特异性影响。在进一步的研究中，我们通过逆行追踪与绘制 IL-1β 诱导的 BNST 和 CeA 细胞中 Fos 增加的图谱相结合，检查了 PVN、BNST 和 CeA 之间的功能联系。就 BNST 而言，这些研究表明全身性 IL-1beta 给药会募集直接投射到 PVN 的腹侧 BNST 细胞。就 CeA 而言，获得的结果与系统性 IL-1β 募集的外侧 CeA 细胞可以调节直接投射到 BNST 的内侧 CeA 细胞的活性的安排一致。总之，目前的研究结果与以下假设一致：BNST 作为 CeA 和 PVN 之间的中继，从而有助于 CeA 调节促垂体 CRF 细胞对全身给予 IL-1β 的反应。 (C) 2003 Wiley-Liss, Inc.
Systemic infection activates the hypothalamic-pituitary-adrenal (HPA) axis, and brainstem catecholamine cells have been shown to contribute to this response. However, recent work also suggests an important role for the central amygdala (CeA). Because direct connections between the CeA and the hypothalamic apex of the HPA axis are minimal, the present study investigated whether the bed nucleus of the stria terminalis (BNST) might act as a relay between them. This was done by using an animal model of acute systemic infection involving intravascular delivery of the proinflammatory cytokine interleukin-1beta (IL-1beta, 1 mug/kg). Unilateral ibotenic acid lesions encompassing the ventral BNST significantly reduced both IL-1beta-induced increases in Fos immunoreactivity in corticotropin-releasing factor (CRF) cells of the hypothalamic paraventricular nucleus (PVN) and corresponding increases in adrenocorticotropic hormone (ACTH) secretion. Similar lesions had no effect on CRF cell responses to physical restraint, suggesting that the effects of BNST lesions were not due to a nonspecific effect on stress responses. In further studies, we examined the functional connections between PVN, BNST, and CeA by combining retrograde tracing with mapping of IL-1beta-induced increases in Fos in BNST and CeA cells. In the case of the BNST, these studies showed that systemic IL-1beta administration recruits ventral BNST cells that project directly to the PVN. In the case of the CeA, the results obtained were consistent with an arrangement whereby lateral CeA cells recruited by systemic IL-1beta could regulate the activity of medial CeA cells projecting directly to the BNST. In conclusion, the present findings are consistent with the hypothesis that the BNST acts as a relay between the CeA and PVN, thereby contributing to CeA modulation of hypophysiotropic CRF cell responses to systemic administration of IL-1beta. (C) 2003 Wiley-Liss, Inc.