Alpha-2A-adrenergic receptors are present on neurons in the central nucleus of the amygdala that project to the dorsal vagal complex in the rat
Alpha-2A-adrenergic receptors are present on neurons in the central nucleus of the amygdala that project to the dorsal vagal complex in the rat
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DOI：
10.1002/syn.10136
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发表时间：
2002-12-15
期刊：
影响因子：
2.3
通讯作者：
Pickel, VM
中科院分区：
文献类型：
--
作者：
Glass, MJ;Colago, EEO;Pickel, VM
杏仁中央核(CEA)和迷走神经背侧复合体(DVC)之间的下行通路是与情绪相关的自主神经功能的重要底物。儿茶酚胺和α-2A型肾上腺素能受体激动剂(α(2A)-AR)可以缓解与厌恶刺激相关的心血管和胃肠道症状，对儿茶酚胺和肾上腺素能受体激动剂的调节作用至关重要。然而，α(2A)-AR在CEA内的亚细胞分布尚不清楚。目前也不知道CEA中是否有表达α(2A)-AR的神经元投射到迷走神经背侧复合体。为了解决这些问题，我们研究了将逆行示踪剂荧光金(FG)微量注射到迷走神经背侧复合体最后区的大鼠CEA中α(2A)-AR的免疫细胞化学标记。最后区是一个涉及心肺和胃肠功能的区域。在CEA的所有α(2A)-AR标记轮廓中，大多数是树突(42%)或体细胞(24%)。α(2A)-AR标记常出现在树突的质膜上，主要分布在胞体内的内体样细胞器中。在所有α(2A)-AR免疫反应阳性胞体中，62%的树突也有FG的免疫标记，23%的树突也有逆行示踪剂的标记。α(2A)-AR在有或无FG的胞体或树突中的分布没有差别。其余单标的α(2A)-AR图谱由轴突(11%)、轴突终末(12%)和神经胶质突起(13%)组成。在许多情况下，α(2A)-AR标记的胶质细胞或轴突终末与DVC投射神经元相对。综上所述，这一证据表明，α(2A)-AR激活的主要部位在CEA神经元树突的突触外部位，其中许多投射到DVC，并显示内体受体标记。此外，这些结果表明，激活CEA中的α(2A)-AR可能通过间接机制影响DVC投射神经元的活动，包括突触前递质释放或神经胶质功能的改变。这些结果表明，CEA中的α(2A)-AR激动剂可能调节许多过程，包括应激诱发的自主神经反应和摄食行为。(C)2002年Wiley-Liss，Inc.
The descending pathway between the central nucleus of the amygdala (CeA) and the dorsal vagal complex (DVC) is an important substrate for autonomic functions associated with emotion. Activity in this circuit is crucially modulated by catecholamines and agonists of the alpha-2A-adrenergic receptor (alpha(2A)-AR), which relieve cardiovascular and gastrointestinal symptoms associated with experience of aversive stimuli. The subcellular distribution of alpha(2A)-AR within the CeA, however, has not been characterized. It is also not known if any alpha(2A)-AR-expressing neurons in the CeA project to the dorsal vagal complex. In order to address these questions, we examined the immunocytochemical labeling of alpha(2A)-AR in the CeA of rats receiving microinjection of the retrograde tracer fluorogold (FG) into the dorsal vagal complex at the level of the area postrema, an area involved in cardiorespiratory and gastrointestinal functions. Of all alpha(2A)-AR-labeled profiles in the CeA, the majority were either dendrites (42%) or somata (24%). alpha(2A)-AR labeling was often present on the plasmalemma in dendrites and was mainly found in endosome-like organelles in somata. Of all alpha(2A)-AR immunoreactive somata, 62% also contained immunolabeling for FG and 23% of all dendrites also showed labeling for the retrograde tracer. The intracellular distribution of alpha(2A)-AR did not differ in somata or dendrites with or without detectable FG. The remaining singly labeled alpha(2A)-AR profiles consisted of axons (11%), axon terminals (12%), and glial processes (13%). In numerous instances, alpha(2A)-AR-labeled glia or axon terminals were apposed to DVC projecting neurons. Together, this evidence suggests that the principal site for alpha(2A)-AR activation is at extrasynaptic sites on dendrites of CeA neurons, many of which project to the DVC and also show endosomal receptor labeling. In addition, these results indicate that activation of alpha(2A)-AR in the CeA may influence the activity of DVC projecting neurons through indirect mechanisms, including changes in presynaptic transmitter release or glial function. These results suggest that alpha(2A)-AR agonists in the CeA may modulate numerous processes including stress-evoked autonomic reactions and feeding behavior. (C) 2002 Wiley-Liss, Inc.