Long-term depression in the superior cervical ganglion of the rat

Alkadhi, Karim A.; Al-Hijailan, Reem S.; Alzoubi, Karem H.

doi:10.1016/j.brainres.2008.07.112

Cited by 7 publications

(5 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…reported that LTD also can be induced in autonomic ganglia. Fifteen minutes of HFS (3–5HZ, 0.3ms duration) at the preganglionic nerve produced a long‐lasting (>3 hours), 20–40% decrease in the amplitude of neuron activity in the superior cervical ganglion of the rat 30 . We hypothesize that the inhibitory effects of LL‐VNS may be in part mediated by LTD‐related mechanisms.…”

Section: Discussionmentioning

confidence: 89%

Low‐Level Vagosympathetic Nerve Stimulation Inhibits Atrial Fibrillation Inducibility: Direct Evidence by Neural Recordings from Intrinsic Cardiac Ganglia

Yu¹,

Scherlag²,

Li³

et al. 2010

Cardiovasc electrophysiol

115

104

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 89%

Low‐Level Vagosympathetic Nerve Stimulation Inhibits Atrial Fibrillation Inducibility: Direct Evidence by Neural Recordings from Intrinsic Cardiac Ganglia

Yu¹,

Scherlag²,

Li³

et al. 2010

Cardiovasc electrophysiol

115

104

View full text Add to dashboard Cite

show abstract

“…Open Sci. 7: 200265 synaptic plasticity, such as long-term potentiation (LTP) and long-term depression (LTD) in the hippocampus [39,40] or in the stellate and superior cervical sympathetic ganglia [41,42]. Neuronal calcium dysregulation, therefore, has the potential to influence the functional connectivity within neuronal networks of both the CNS and ANS along the neuro-cardiac axis.…”

Section: Neuro-cardiac Physiology and Diseasementioning

confidence: 99%

“…Calcium dysregulation underlies many cardiovascular pathologies such as hypertrophy [ 32 , 33 ], hypertension [ 34 , 35 ] and arrhythmias [ 36 – 38 ]. In the central nervous system (CNS) and peripheral nervous system (PNS), calcium is involved in neurotransmitter release, generation of excitatory or inhibitory postsynaptic potentials and the induction of different forms of synaptic plasticity, such as long-term potentiation (LTP) and long-term depression (LTD) in the hippocampus [ 39 , 40 ] or in the stellate and superior cervical sympathetic ganglia [ 41 , 42 ]. Neuronal calcium dysregulation, therefore, has the potential to influence the functional connectivity within neuronal networks of both the CNS and ANS along the neuro-cardiac axis.…”

Section: Neuro-cardiac Physiology and Diseasementioning

confidence: 99%

Combining tissue engineering and optical imaging approaches to explore interactions along the neuro-cardiac axis

et al. 2020

View full text Add to dashboard Cite

Interactions along the neuro-cardiac axis are being explored with regard to their involvement in cardiac diseases, including catecholaminergic polymorphic ventricular tachycardia, hypertension, atrial fibrillation, long QT syndrome and sudden death in epilepsy. Interrogation of the pathophysiology and pathogenesis of neuro-cardiac diseases in animal models present challenges resulting from species differences, phenotypic variation, developmental effects and limited availability of data relevant at both the tissue and cellular level. By contrast, tissue-engineered models containing cardiomyocytes and peripheral sympathetic and parasympathetic neurons afford characterization of cellular- and tissue-level behaviours while maintaining precise control over developmental conditions, cellular genotype and phenotype. Such approaches are uniquely suited to long-term, high-throughput characterization using optical recording techniques with the potential for increased translational benefit compared to more established techniques. Furthermore, tissue-engineered constructs provide an intermediary between whole animal/tissue experiments and in silico models. This paper reviews the advantages of tissue engineering methods of multiple cell types and optical imaging techniques for the characterization of neuro-cardiac diseases.

show abstract

“…In the stellate and superior cervical sympathetic ganglia that innervate the heart, short-term increases in the strength of synaptic transmission occur in response to a single action potential or a short train of impulses (Bennett et al, 1976 ; Lin et al, 1998 ), and longer bursts of high frequency stimulation of the preganglionic nerve result in enhancement of postsynaptic responses and heart rate (Alonso-deFlorida et al, 1991 ; Bachoo and Polosa, 1991 ; Aileru et al, 2004 ). Conversely, low frequency stimulation can induce LTD (Alkadhi et al, 2008 ). Induction of ganglionic LTP and LTD (gLTP/gLTD) is not dependent on transmission via nicotinic, adrenergic, muscarinic or adenosine receptors, but requires activation of 5-HT 3 receptors by serotonin, potentially released from SIF cells (Alkadhi et al, 1996 , 2008 ).…”

Section: Beyond the Brain – Does Synaptic Plasticity Occur In Neuronsmentioning

confidence: 99%

“…Conversely, low frequency stimulation can induce LTD (Alkadhi et al, 2008 ). Induction of ganglionic LTP and LTD (gLTP/gLTD) is not dependent on transmission via nicotinic, adrenergic, muscarinic or adenosine receptors, but requires activation of 5-HT 3 receptors by serotonin, potentially released from SIF cells (Alkadhi et al, 1996 , 2008 ). Both pre- and postsynaptic expression mechanisms have been implicated in gLTP (Alkadhi et al, 2005 ), with increases in evoked acetylcholine (ACh) release (Briggs et al, 1985 ) and postsynaptic sensitivity to ACh observed (Bachoo and Polosa, 1991 ).…”

Section: Beyond the Brain – Does Synaptic Plasticity Occur In Neuronsmentioning

confidence: 99%

Synaptic Plasticity in Cardiac Innervation and Its Potential Role in Atrial Fibrillation

et al. 2018

View full text Add to dashboard Cite

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.

show abstract

Long-term depression in the superior cervical ganglion of the rat

Cited by 7 publications

References 42 publications

Low‐Level Vagosympathetic Nerve Stimulation Inhibits Atrial Fibrillation Inducibility: Direct Evidence by Neural Recordings from Intrinsic Cardiac Ganglia

Low‐Level Vagosympathetic Nerve Stimulation Inhibits Atrial Fibrillation Inducibility: Direct Evidence by Neural Recordings from Intrinsic Cardiac Ganglia

Combining tissue engineering and optical imaging approaches to explore interactions along the neuro-cardiac axis

Synaptic Plasticity in Cardiac Innervation and Its Potential Role in Atrial Fibrillation

Contact Info

Product

Resources

About