Glass Michael J, Colago Eric E O, Pickel Virginia M
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA.
Synapse. 2002 Dec 15;46(4):258-68. doi: 10.1002/syn.10136.
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.
杏仁核中央核（CeA）与迷走神经背核复合体（DVC）之间的下行通路是与情绪相关的自主功能的重要基础。该神经回路中的活动受到儿茶酚胺和α-2A肾上腺素能受体（α(2A)-AR）激动剂的关键调节，这些物质可缓解与厌恶刺激体验相关的心血管和胃肠道症状。然而，CeA内α(2A)-AR的亚细胞分布尚未明确。CeA中是否有任何表达α(2A)-AR的神经元投射到迷走神经背核复合体也不清楚。为了解决这些问题，我们检测了在最后区水平将逆行示踪剂荧光金（FG）显微注射到迷走神经背核复合体的大鼠CeA中α(2A)-AR的免疫细胞化学标记。在CeA中所有α(2A)-AR标记的形态中，大多数是树突（42%）或胞体（24%）。α(2A)-AR标记通常出现在树突的质膜上，主要存在于胞体的内体样细胞器中。在所有α(2A)-AR免疫反应性胞体中，62%也含有FG免疫标记，所有树突的23%也显示有逆行示踪剂标记。有或没有可检测到的FG的胞体或树突中，α(2A)-AR的细胞内分布没有差异。其余单独标记的α(2A)-AR形态包括轴突（11%）、轴突终末（12%）和胶质细胞突起（13%）。在许多情况下，α(2A)-AR标记的胶质细胞或轴突终末与投射到DVC的神经元相邻。总之，这些证据表明α(2A)-AR激活的主要部位是CeA神经元树突的突触外位点，其中许多投射到DVC，并且也显示有内体受体标记。此外，这些结果表明CeA中α(2A)-AR的激活可能通过间接机制影响投射到DVC的神经元的活动，包括突触前递质释放或胶质细胞功能的变化。这些结果表明CeA中的α(2A)-AR激动剂可能调节包括应激诱发的自主反应和摄食行为在内的许多过程。
