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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Amygdalar and prefrontal pathways to the lateral hypothalamus are activated by a learned cue that stimulates eating.
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Amygdalar and prefrontal pathways to the lateral hypothalamus are activated by a learned cue that stimulates eating.

机译：到下丘脑外侧的杏仁核和前额叶通路被刺激进食的学习线索激活。

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Experimental animals that are trained to associate a cue with food consumption when hunger prevails will subsequently consume a greater amount of food when that cue is presented under conditions of satiety. Previously, we showed that this phenomenon of conditioned potentiation of feeding is abolished by a neurotoxic lesion that encompasses the basolateral (BL), basomedial (BM), and lateral (LA) nuclei of the amygdala (AMY) and by disconnection of this region and lateral hypothalamus (LHA). Here, we combined immediate-early gene (IEG) and tract-tracing methods to map functional AMY-LHA circuitry that is engaged when potentiated feeding is produced by pavlovian conditioning. Sated rats were assessed for food consumption in the presence of a cue that was paired previously with food (CS+), or in the presence of another cue that was never paired with food (CS-), in two consecutive tests temporally arranged for activation of the effector IEGs Arc (activity-regulated cytoskeletal protein) and Homer 1a. We examined the selective induction of the IEGs by tests with CS+ or CS- presentations in AMY neurons that project to LHA, as identified with the retrograde tracer FluoroGold. Using the same labeling methods, we also examined neurons in several other forebrain regions, including the prefrontal cortex and nucleus accumbens, that receive strong inputs from BL/BM/LA nuclei and, in turn, innervate the LHA. Our results indicate that a cue that has acquired the ability to promote eating in sated rats (CS+) strongly activates a functional network formed by direct pathways from the BL/BM and orbitomedial prefrontal cortex to the LHA.
机译：当饥饿感盛行时，受过训练将提示与食物消耗相关联的实验动物随后将在饱足条件下出现该提示时消耗大量食物。以前，我们表明，通过覆盖杏仁核（AMY）的基底外侧（BL），基底体（BM）和外侧（LA）核的神经毒性病变以及该区域的断开连接，可以消除这种条件化进食增强的现象。下丘脑外侧（LHA）。在这里，我们结合了立即早期基因（IEG）和管道追踪方法来绘制功能性AMY-LHA电路，当通过巴甫洛夫式条件产生强化进食时，该功能会参与。在时间上安排了两个时间连续激活的连续测试中，在存在先前与食物配对的提示（CS +）或存在从未与食物配对的另一个提示（CS-）的情况下评估了饱足大鼠的食物消耗。效应IEGs Arc（活性调节的细胞骨架蛋白）和Homer 1a。我们通过对投射到LHA的AMY神经元中的CS +或CS-呈递进行了测试，检查了IEG的选择性诱导，如逆行示踪剂FluoroGold所鉴定的。使用相同的标记方法，我们还检查了其他几个前脑区域的神经元，包括前额叶皮层和伏隔核，它们从BL / BM / LA核中获得大量输入，进而支配LHA。我们的结果表明，已经获得了在饱足大鼠（CS +）中促进进食的能力的线索会强烈激活由BL / BM和眶额前额叶皮层到LHA的直接途径形成的功能网络。

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