Neural controls of prostaglandin 2 pyrogenic, tachycardic, and anorexic actions are anatomically distributed.
Neural controls of prostaglandin 2 pyrogenic, tachycardic, and anorexic actions are anatomically distributed.
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DOI：
10.1210/en.2010-1309
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发表时间：
2011-03
期刊：
影响因子：
4.8
通讯作者：
K. Skibicka;A. Alhadeff;T. Leichner;H. Grill
中科院分区：
文献类型：
--
作者：
K. Skibicka;A. Alhadeff;T. Leichner;H. Grill
发烧和厌食症是由免疫系统受到挑战引起的。因为这些反应在短时间内是自适应的，但在长时间内是有害的，所以了解调节神经回路是很重要的。前列腺素（PGE）是这些免疫反应的关键信号元件。尽管PGE受体在整个大脑中广泛分布，但研究主要集中在下丘脑视前区作为PGE作用的介导部位。下丘脑室旁核（PVH）、臂旁核（PBN）和孤束核（NTS）神经元也表达PGE受体，并在全身性病原体感染时被激活。这些神经元在pge诱导的发热、心动过速和厌食症中的作用尚未被探索，这是本报告的主题。将一定剂量的pge2微注射到第三或第四脑室(v)，或直接注射到PVH背侧、PBN外侧和NTS内侧，并在清醒、行为正常的大鼠中测量核心和棕色脂肪组织温度、心率、运动活动和食物摄入量。pge2递送至多个脑部位（第三或第四v、PVH或PBN）可引起短潜伏期（< 10分钟）发热和心动过速。相比之下，只有在第三次v和PVH刺激时才会出现厌食效应。NTS PGE 2刺激无效果；任何部位的运动活动都没有受到影响。这些数据与pge2诱导效应的观点是一致的，pge2诱导效应是由解剖学上分布的位点介导的，而不是单一的中心。这些数据还强调了介导pge2的热原和厌食作用的神经通路的潜在解剖解离。
Fever and anorexia are induced by immune system challenges. Because these responses are adaptive when short lasting but deleterious when prolonged, an understanding of the mediating neural circuitry is important. Prostaglandins (PGE) are a critical signaling element for these immune responses. Despite the widespread distribution of PGE receptors throughout the brain, research focuses on the hypothalamic preoptic area as the mediating site of PGE action. Paraventricular nucleus of the hypothalamus (PVH), parabrachial nucleus (PBN), and nucleus tractus solitarius (NTS) neurons also express PGE receptors and are activated during systemic pathogen infection. A role for these neurons in PGE-induced fever, tachycardia, and anorexia is unexplored and is the subject of this report. A range of PGE₂ doses was microinjected into third or fourth ventricles (v), or directly into the dorsal PVH, lateral PBN, and medial NTS, and core and brown adipose tissue temperature, heart rate, locomotor activity, and food intake were measured in awake, behaving rats. PGE₂ delivery to multiple brain sites (third or fourth v, PVH, or PBN) induced a short- latency (< 10 min) fever and tachycardia. By contrast, an anorexic effect was observed only in response to third v and PVH stimulation. NTS PGE₂ stimulation was without effect; locomotor activity was not affected for any of the sites. The data are consistent with a view of PGE₂-induced effects as mediated by anatomically distributed sites rather than a single center. The data also underscore a potential anatomical dissociation of the neural pathways mediating pyrogenic and anorexic effects of PGE₂.