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首页> 美国卫生研究院文献>American Journal of Physiology - Regulatory Integrative and Comparative Physiology >Neural Integration of Peripheral Signals Implicated in the Control of Energy Homeostasis and Metabolism: The role of hypothalamic ingestive behavior controllers in generating dehydration anorexia: a Fos mapping study
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Neural Integration of Peripheral Signals Implicated in the Control of Energy Homeostasis and Metabolism: The role of hypothalamic ingestive behavior controllers in generating dehydration anorexia: a Fos mapping study

机译：能量平衡和代谢控制中涉及的周围信号的神经整合：下丘脑的摄取行为控制器在产生脱水性厌食症中的作用：Fos作图研究

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Giving rats 2.5% saline to drink for 3–5 days simply and reliably generates anorexia. Despite having the neurochemical and hormonal markers of negative energy balance, dehydrated anorexic rats show a marked suppression of spontaneous food intake, as well as the feeding that is usually stimulated by overnight starvation or a 2-deoxy-d-glucose (2DG) challenge. These observations are consistent with a dehydration-dependent inhibition of the core circuitry that controls feeding. We hypothesize that this inhibition is directed at those neurons in the paraventricular nucleus and lateral hypothalamic area that constitute the hypothalamic “behavior controller” for feeding rather than their afferent inputs from the arcuate nucleus or hindbrain that convey critical feeding-related sensory information. To test this hypothesis, we mapped and quantified the Fos-immunoreactive response to 2DG in control and dehydrated rats drinking 2.5% saline. Our rationale was that regions showing an attenuated Fos response to 2DG in dehydrated animals would be strong candidates as the targets of dehydration-induced suppression of 2DG feeding. We found that the Fos response to combined dehydration and 2DG was attenuated only in the lateral hypothalamic area, with dehydration alone increasing Fos in the lateral part of the paraventricular nucleus. In the arcuate nucleus and those regions of the hindbrain that provide afferent inputs critical for the feeding response to 2DG, the Fos response to 2DG was unaffected by dehydration. Therefore, dehydration appears to target the lateral hypothalamic area and possibly the lateral part of the paraventricular nucleus to suppress the feeding response to 2DG.
机译：简单可靠地给大鼠2.5％的盐水喝3-5天会产生厌食。尽管有神经化学和激素标记的负能量平衡，脱水的厌食症大鼠仍表现出明显的自发性食物摄入抑制，以及通常由过夜饥饿或2-脱氧-d-葡萄糖（2DG）刺激刺激的进食。这些观察结果与控制饲喂的核心电路的脱水依赖性抑制作用相一致。我们假设这种抑制作用针对的是构成下丘脑进食的“行为控制者”的脑室旁核和下丘脑外侧区域的神经元，而不是它们的弓形核或后脑的传入输入，它们传达了与进食有关的重要感觉信息。为了检验该假设，我们在饮用2.5％盐水的对照组和脱水大鼠中绘制并量化了对2DG的Fos免疫反应性。我们的理由是，脱水动物中对2DG的Fos响应减弱的区域将很可能成为脱水诱导抑制2DG进食的目标。我们发现，仅在下丘脑外侧区域，Fos对脱水和2DG的反应减弱，而单独脱水会增加脑室旁核外侧区域的Fos。在弓形核和后脑的那些区域，这些区域提供对2DG的饲喂反应至关重要的传入输入，对2DG的Fos反应不受脱水的影响。因此，脱水似乎是针对下丘脑外侧区域，甚至可能是脑室旁核的外侧部分，以抑制对2DG的进食反应。

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