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首页> 外文期刊>The European Journal of Neuroscience >C1 Neurons in the RVLM: Are they catecholaminergic in name only? (Commentary on Abbott et al.)
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C1 Neurons in the RVLM: Are they catecholaminergic in name only? (Commentary on Abbott et al.)

机译：RVLM中的C1神经元：它们仅是儿茶酚胺能名吗？ （关于雅培等人的评论）

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摘要

Catecholaminergic neurons in the rostral ventrolateral medulla (RVLM), also known as the Cl cell group, are known to play an important role in the generation and control of sympathetic activity (Card et ah, 2006). Many of these Cl neurons, as well as neighboring non-catechol-aminergic neurons in the RVLM, monosynaptically project to the intermediolateral column of the spinal cord and provide the primary tonic excitatory drive to sympathetic vasomotor and cardiac neurons (Guyenet et ah, 2013). RVLM Cl neurons also send projections to many other centers involved in respiratory and autonomic function including the dorsal vagal motor nucleus (DePuy et ah, 2013). Here, in this veiy comprehensive and interesting study conducted by Abbott et al. (2013), the authors crossbred mice to produce progeny in which dopamine-(3-hydroxylase-containing neurons lacked the glutamate transporter VGLUT2, a transporter responsible for the sequestration of the excitatoiy neurotransmitter glutamate into synaptic vesicles in these neurons. Furthermore, Cl neurons in these animals could be selectively activated in vivo using optogenetic stimulation of expressed channelrhodopsin-2 (ChR2) following microinjection of a floxed ChR2-expressing virus into the RVLM. Selective photostimulation of the Cl neurons increased respiratory frequency in control animals with unaltered VGLUT2 expression, but in mice with VGLUT2 deficiencies in catecholaminergic neurons the responses upon Cl photoactivation were absent. Similarly, the activation of vagal fibers upon photoactivation of Cl neurons was blunted or absent in animals with VGLUT2 deficiencies. This work, taken together with previous work from this group and others, indicates that catecholaminergic neurons in the RVLM use glutamate primarily, if not exclusively, as a transmitter to influence downstream autonomic and respiratory neurons (Morrison, 2003; Guyenet et ah, 2013). This well-founded conclusion raises the issue, are these neurons catecholaminergic in name only? Three potential unexplored roles for catecholamine synthesis in these neurons are that catecholamines are co-released from the synapses of these neurons but do not act on their anticipated postsynaptic neuronal targets but rather alter glial or other non-neuronal targets. Alternatively, catecholamines might only be syn-aptically co-released from these neurons upon challenges to the autonomic and/or respiratory systems or in disease states. This, while possible, seems unlikely as these investigators stimulated Cl neurons with a range of activation paradigms. Another interesting and yet untested hypothesis is that catecholamines are released not at the synapse but at the soma or dendrites of Cl neurons to serve in a role distinctly different from fast neurotransmission (Sevigny et ah, 2008). This important study demonstrates the powerful influence of the glutamatergic projections of these Cl neurons on respiratory and autonomic function, but why they are catecholaminergic remains unknown.
机译：鼻侧腹外侧延髓（RVLM）中的儿茶酚胺能神经元（也称为Cl细胞群）在交感神经活动的产生和控制中起着重要作用（Card等人，2006）。这些Cl神经元中的许多以及RVLM中相邻的非儿茶酚胺能神经元单突触地投射到脊髓的中间外侧柱上，并为交感性血管舒缩和心脏神经元提供主要的兴奋性兴奋驱动力（Guyenet等，2013）。 。 RVLM C1神经元还向与呼吸和自主功能有关的许多其他中心发送预测，包括迷走神经背运动核（DePuy等，2013）。在这里，雅培等人进行了这项全面而有趣的研究。 （2013），这组作者杂交了小鼠以产生后代，其中多巴胺-（3-羟化酶）的神经元缺乏谷氨酸转运蛋白VGLUT2，谷氨酸转运蛋白负责将兴奋性神经递质谷氨酸螯合在这些神经元的突触小泡中。在向RVLM中显微注射一种表达ChR2的浮游性病毒后，可以通过光遗传刺激表达的Channelrhodopsin-2（ChR2）在体内选择性激活这些动物体内的C1神经元的选择性光刺激。但是在儿茶酚胺能神经元中存在VGLUT2缺陷的小鼠中，缺乏Cl的光激活反应;同样，在具有VGLUT2缺陷的动物中，Cl神经元的光激活时迷走神经纤维的激活也变钝或缺失。等表明儿茶酚胺能神经元在RVLM中，谷氨酸主要（如果不是排他性的话）主要用作影响下游自主神经和呼吸神经元的传递因子（Morrison，2003; Guyenet等人，2013年）。这个有根据的结论提出了一个问题，这些神经元仅仅是儿茶酚胺能的吗？儿茶酚胺合成在这些神经元中的三个潜在的尚未探索的作用是儿茶酚胺从这些神经元的突触中共释放，但不作用于其预期的突触后神经元靶标，而是改变神经胶质或其他非神经元靶标。或者，儿茶酚胺可能仅在对自主和/或呼吸系统的挑战或处于疾病状态时才从这些神经元突触共释放。由于这些研究人员以一系列激活范例刺激了Cl神经元，因此这似乎不太可能。另一个有趣但未经检验的假设是儿茶酚胺不是在突触中释放，而是在Cl神经元的体细胞或树突中释放，起着与快速神经传递明显不同的作用（Sevigny等，2008）。这项重要的研究证明了这些Cl神经元的谷氨酸能投射对呼吸和自主神经功能的强大影响，但是为什么它们是儿茶酚胺能的仍然未知。

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