Synaptic Plasticity in Cardiac Innervation and Its Potential Role in Atrial Fibrillation.
Synaptic Plasticity in Cardiac Innervation and Its Potential Role in Atrial Fibrillation.
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心脏神经支配中的突触可塑性及其在心房颤动中的潜在作用。
DOI：
10.3389/fphys.2018.00240
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发表时间：
2018
影响因子：
4
通讯作者：
Montgomery JM
中科院分区：
文献类型：
--
作者：
Ashton JL;Burton RAB;Bub G;Smaill BH;Montgomery JM
突触可塑性被定义为突触改变其传递强度的能力。大脑中突触连接的可塑性是神经科学研究的主要焦点，因为它是支撑学习和记忆的主要机制。然而，在大脑之外，外周神经元的可塑性还不太清楚，特别是支配心脏的神经元。心房接受来自周围神经系统的自主分支的丰富的神经支配。交感神经元聚集在脊髓旁的星状神经节和颈神经节中，并将纤维延伸到心脏，直接支配心肌。这些神经元是在心脏病、室性心律失常和心脏性猝死中观察到的交感神经活动过度活跃的主要驱动因素。已经观察到突触前和突触后变化都发生在交感神经节神经元形成的突触处，这表明交感神经-心脏突触处的可塑性是心律失常的主要原因。对心脏表面簇状分布的副交感神经元的可塑性知之甚少。这些神经元簇，称为神经节丛，或“小大脑”，可以独立地调节心脏的神经控制，增强其兴奋性的刺激可以诱导心律失常，如心房纤颤。这些神经元改变副交感神经活动的能力表明，可塑性可能确实发生在神经节丛神经元上和神经节丛神经元形成的突触。这种变化不仅可以微调心脏的自主神经支配，但也可能是一个来源，适应不良的可塑性在心房颤动。
Synaptic plasticity is defined as the ability of synapses to change their strength of transmission. Plasticity of synaptic connections in the brain is a major focus of neuroscience research, as it is the primary mechanism underpinning learning and memory. Beyond the brain however, plasticity in peripheral neurons is less well understood, particularly in the neurons innervating the heart. The atria receive rich innervation from the autonomic branch of the peripheral nervous system. Sympathetic neurons are clustered in stellate and cervical ganglia alongside the spinal cord and extend fibers to the heart directly innervating the myocardium. These neurons are major drivers of hyperactive sympathetic activity observed in heart disease, ventricular arrhythmias, and sudden cardiac death. Both pre- and postsynaptic changes have been observed to occur at synapses formed by sympathetic ganglion neurons, suggesting that plasticity at sympathetic neuro-cardiac synapses is a major contributor to arrhythmias. Less is known about the plasticity in parasympathetic neurons located in clusters on the heart surface. These neuronal clusters, termed ganglionated plexi, or “little brains,” can independently modulate neural control of the heart and stimulation that enhances their excitability can induce arrhythmia such as atrial fibrillation. The ability of these neurons to alter parasympathetic activity suggests that plasticity may indeed occur at the synapses formed on and by ganglionated plexi neurons. Such changes may not only fine-tune autonomic innervation of the heart, but could also be a source of maladaptive plasticity during atrial fibrillation.
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影响因子：
5.5
作者：
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