Department of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, 43 Szigony St, Budapest, 1083, Hungary.
Neuroendocrinology Program, Semmelweis University Neurosciences Doctoral School, Budapest, Hungary.
Brain Struct Funct. 2018 Jan;223(1):391-414. doi: 10.1007/s00429-017-1501-4. Epub 2017 Aug 29.
Following fasting, satiety is accompanied by neuronal activation in brain areas including the central amygdalar nucleus (CEA). Since CEA is known to inhibit food intake, we hypothesized that CEA contributes to the termination of meal during refeeding. To better understand the organization of this satiety-related circuit, the interconnections of the CEA with refeeding-activated neuronal groups were elucidated using retrograde (cholera toxin-β subunit, CTB) and anterograde (phaseolus vulgaris leucoagglutinin, PHA-L) tracers in male rats. C-Fos-immunoreactivity was used as marker of neuronal activation. The refeeding-activated input of the CEA primarily originated from the paraventricular thalamic, parasubthalamic and parabrachial nuclei. Few CTB-c-Fos double-labeled neurons were detected in the prefrontal cortex, lateral hypothalamic area, nucleus of the solitary tract (NTS) and the bed nuclei of the stria terminalis (BNST). Only few refeeding-activated proopiomelanocortin-producing neurons of the arcuate nucleus projected to the CEA. Anterograde tract tracing revealed a high density of PHAL-labeled axons contacted with refeeding-activated neurons in the BNST, lateral hypothalamic area, parasubthalamic, paraventricular thalamic and parabrachial nuclei and NTS; a low density of labeled axons was found in the paraventricular hypothalamic nucleus. Chemogenetic activation of the medial CEA (CEAm) inhibited food intake during the first hour of refeeding, while activation of lateral CEA had no effect. These data demonstrate the existence of reciprocal connections between the CEA and distinct refeeding-activated hypothalamic, thalamic and brainstem nuclei, suggesting the importance of short feedback loops in the regulation of satiety and importance of the CEAm in the regulation of food intake during refeeding.
禁食后，饱食伴随着包括中央杏仁核（CEA）在内的大脑区域神经元的激活。由于已知 CEA 抑制食物摄入，我们假设 CEA 有助于在重新进食时终止进食。为了更好地理解这个与饱腹感相关的回路的组织，使用逆行（霍乱毒素-β亚基，CTB）和顺行（菜豆植物凝集素，PHA-L）示踪剂在雄性大鼠中阐明了 CEA 与重新进食激活的神经元群之间的相互连接。C-Fos 免疫反应性被用作神经元激活的标志物。CEA 的重新进食激活输入主要来自室旁丘脑、旁下丘脑和臂旁核。在额皮质、外侧下丘脑区域、孤束核（NTS）和终纹床核（BNST）中检测到很少的 CTB-c-Fos 双标记神经元。只有少数弓状核产生促黑皮质素原的重新进食激活神经元投射到 CEA。顺行束追踪显示 BNST、外侧下丘脑区域、旁下丘脑、室旁丘脑和臂旁核以及 NTS 中与重新进食激活神经元接触的 PHAL 标记轴突密度很高；在室旁下丘脑核中发现标记轴突密度较低。内侧 CEA（CEAm）的化学遗传激活抑制了重新进食后第一小时的食物摄入，而外侧 CEA 的激活没有影响。这些数据表明 CEA 与不同的重新进食激活的下丘脑、丘脑和脑干核之间存在相互联系，这表明短反馈回路在饱腹感调节中的重要性以及 CEAm 在重新进食期间食物摄入调节中的重要性。
