Abstract
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.
Highlights
Cardiac arrhythmias are devastating disorders in which normal sinus rhythm is disrupted, resulting in the heart beating too rapidly, slowly, or erratically, thereby impairing cardiac function
It is thought to be proarrhythmic by enhancing delayed afterdepolarisation related ectopic activity through increasing β-adrenoceptor-dependent diastolic Ca2+ leak (Dobrev et al, 2011), and stabilizing re-entrant activity by reducing atrial action potential duration through increased acetylcholine-dependent K+ current (Kneller et al, 2002)
Atrial sympathetic hyperinnervation and remodeling of the autonomic nervous system are both contributors to positive feedback loops that promote persistent and recurrent atrial fibrillation (AF) (Gould et al, 2006; Tan et al, 2008; Chou and Chen, 2009; Iwasaki et al, 2011)
Summary
Cardiac arrhythmias are devastating disorders in which normal sinus rhythm is disrupted, resulting in the heart beating too rapidly, slowly, or erratically, thereby impairing cardiac function. In persistent AF, atrial electrical and structural remodeling amplifies the electrophysiological instability that drives AF and the re-entrant substrates that sustain it (Iwasaki et al, 2011). Atrial sympathetic hyperinnervation and remodeling of the autonomic nervous system are both contributors to positive feedback loops that promote persistent and recurrent AF (Gould et al, 2006; Tan et al, 2008; Chou and Chen, 2009; Iwasaki et al, 2011). It is argued that progressive remodeling of the atrial neural plexus in persistent AF contributes to the maintenance of electrical instability (Chen et al, 2010, 2014; Shen et al, 2012).
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