Neuronal connections of the central amygdalar nucleus with refeeding-activated brain areas in rats.
Neuronal connections of the central amygdalar nucleus with refeeding-activated brain areas in rats.
复制标题
大鼠中央杏仁核与再进食激活大脑区域的神经元连接。
DOI：
10.1007/s00429-017-1501-4
复制
发表时间：
2018
影响因子：
3.1
通讯作者：
Fekete,Csaba
中科院分区：
文献类型：
--
作者：
Zséli,Györgyi;Vida,Barbara;Szilvásy-Szabó,Anett;Tóth,Mónika;Lechan,RonaldM;Fekete,Csaba
禁食后，饱腹感伴随着包括中央杏仁核（CEA）在内的大脑区域的神经元激活。由于已知CEA抑制食物摄入，我们假设CEA有助于在再喂养期间终止进餐。为了更好地理解这种饱腹感相关回路的组织，使用逆行（霍乱毒素-β亚基，CTB）和顺行（菜豆白细胞凝集素，PHA-L）示踪剂在雄性大鼠中阐明了CEA与再喂养激活的神经元组的相互联系。C-Fos免疫反应性被用作神经元活化的标志物。再喂养激活的CEA输入主要来自丘脑室旁核、丘脑底旁核和臂旁核。在前额叶皮质、下丘脑外侧区、孤束核（NTS）和终纹床核（BNST）中检测到少量CTB-c-Fos双标记神经元。弓状核只有少数再摄食激活的阿黑皮素原产生神经元投射到CEA。顺行束追踪显示，高密度的PHAL标记的轴突接触再喂养激活的神经元在BNST，下丘脑外侧区，丘脑旁，丘脑室旁核和臂旁核和NTS;标记的轴突低密度被发现在下丘脑室旁核。化学发生激活的内侧CEA（CEAm）抑制食物的摄入量在第一个小时的再喂养，而激活的外侧CEA没有影响。这些数据表明，CEA和不同的再喂养激活的下丘脑，丘脑和脑干核之间存在相互联系，这表明短反馈回路的饱腹感的调节和重要性的CEAm在再喂养期间的食物摄入量的调节的重要性。
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.