Ashton Jesse L, Burton Rebecca A B, Bub Gil, Smaill Bruce H, Montgomery Johanna M
Department of Physiology, University of Auckland, Auckland, New Zealand.
Department of Pharmacology, Oxford University, Oxford, United Kingdom.
Front Physiol. 2018 Mar 20;9:240. doi: 10.3389/fphys.2018.00240. eCollection 2018.
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.
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，因为它是学习和记忆的主要支撑机制。然而，在大脑之外，外周神经元的可塑性了解较少，特别是在支配心脏的神经元中。心房接受来自外周神经系统自主分支的丰富神经支配。交感神经元聚集在脊髓旁的星状神经节和颈神经节中，并将纤维延伸至心脏，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亢进的主要驱动因素。在交感神经节神经元形成的突触处，已观察到突触前和突触后都发生了变化，这表明交感神经 - 心脏突触的可塑性是心律失常的主要促成因素。对于位于心脏表面丛集的副交感神经元的可塑性了解较少。这些神经元丛集，称为神经节丛，或“小脑”，可以独立调节心脏的神经控制，增强其兴奋性的刺激可诱发心律失常，如心房颤动。这些神经元改变副交感神经活动的能力表明，在神经节丛神经元形成的突触处确实可能发生可塑性。这种变化不仅可能微调心脏的自主神经支配，而且可能是心房颤动期间适应性不良可塑性的一个来源。
