Abstract

One of the important mechanisms of cardiac regulation is realized via sympathetic innervation of cardiac myocytes. Axons of the sympathetic neurons branch out and form varicosities along their length, filled with synaptic vesicles that contain a major neurotransmitter (norepinephrine) and co-neurotransmitters. The varicosities may closely contact with cardiomyocytes and form neuro-cardiac junctions (NCJs), which have a synapse-like organization, namely pre- and postsynaptic regions separated by a narrow gap. These synaptic structures demonstrate high plasticity, while neurotransmitter release from the presynaptic varicosity is tightly regulated, including due to autoreceptors. Neurotransmission via NCJs mediates fast chronotropic and inotropic effects and also controls tropic processes, which determine the size of cardiomyocytes and the architecture of the heart wall. Different subtypes of postsynaptic adrenoceptors are involved in these short- and long-term effects of neuro-cardiac interactions. Changes in cardiac adrenergic neurotransmission often accompany many widespread pathologies, such as heart failure, arrhythmias and hypertension, contributing to their progression. In this review, we systematized and summarized experimental evidence supporting the hypothesis about cardiac quasi-synaptic transmission that may be of decisive importance for brain-heart communication.

中文翻译：

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神经-心脏交界处在心脏交感神经调节中的作用

摘要

心脏调节的重要机制之一是通过心肌细胞的交感神经支配来实现的。交感神经元的轴突分支并沿其长度形成静脉曲张，充满突触小泡，突触小泡包含主要神经递质（去甲肾上腺素）和共神经递质。静脉曲张可能与心肌细胞紧密接触并形成神经-心脏接头（NCJ），其具有突触样组织，即由狭窄间隙隔开的突触前和突触后区域。这些突触结构表现出高可塑性，而突触前静脉曲张的神经递质释放受到严格调节，包括由于自身受体。通过 NCJs 的神经传递介导快速变时性和肌力作用，并控制热带过程，这决定了心肌细胞的大小和心脏壁的结构。不同亚型的突触后肾上腺素能受体参与这些神经-心脏相互作用的短期和长期影响。心脏肾上腺素能神经传递的变化通常伴随着许多广泛的病理，例如心力衰竭、心律失常和高血压，导致它们的进展。在这篇综述中，我们系统化并总结了支持心脏准突触传递假说的实验证据，该假说可能对脑-心交流具有决定性意义。如心力衰竭、心律失常和高血压，促进其进展。在这篇综述中，我们系统化并总结了支持心脏准突触传递假说的实验证据，该假说可能对脑-心交流具有决定性意义。如心力衰竭、心律失常和高血压，促进其进展。在这篇综述中，我们系统化并总结了支持心脏准突触传递假说的实验证据，该假说可能对脑-心交流具有决定性意义。