ArticleExperimental physiology2010
Infarction-induced cytokines cause local depletion of tyrosine hydroxylase in cardiac sympathetic nerves.
Article in Experimental physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Molecular and cellular neurocardiology in heart disease.The Journal of physiology · 2025Review
- Hypertension-induced heart failure disrupts cardiac sympathetic innervation.American journal of physiology. Heart and circulatory physiology · 2024Article
- Chronic nicotine exposure is associated with electrophysiological and sympathetic remodeling in the intact rabbit heart.American journal of physiology. Heart and circulatory physiology · 2024Article
- Ischemia-reperfusion myocardial infarction induces remodeling of left cardiac-projecting stellate ganglia neurons.American journal of physiology. Heart and circulatory physiology · 2024Article
- Therapeutics That Promote Sympathetic Reinnervation Modulate the Inflammatory Response After Myocardial Infarction.JACC. Basic to translational science · 2022Article
- Article
- Lack of Macrophage Migration Inhibitory Factor Reduces Susceptibility to Ventricular Arrhythmias During the Acute Phase of Myocardial Infarction.Journal of inflammation research · 2021Article
- Cardiac sympathetic nerve transdifferentiation reduces action potential heterogeneity after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2020Article
- Age-related changes in cardiac electrophysiology and calcium handling in response to sympathetic nerve stimulation.The Journal of physiology · 2018Article
- Systemic Inhibition of CREB is Well-tolerated in vivo.Scientific reports · 2016Article
- Molecular and cellular neurocardiology: development, and cellular and molecular adaptations to heart disease.The Journal of physiology · 2016Review
- Myocardial Infarction Causes Transient Cholinergic Transdifferentiation of Cardiac Sympathetic Nerves via gp130.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias.Nature communications · 2015Article
- Dynamic remodeling of the guinea pig intrinsic cardiac plexus induced by chronic myocardial infarction.Autonomic neuroscience : basic & clinical · 2014Article
- Physical (in)activity-dependent structural plasticity in bulbospinal catecholaminergic neurons of rat rostral ventrolateral medulla.The Journal of comparative neurology · 2014Article
- Sympathetic denervation of peri-infarct myocardium requires the p75 neurotrophin receptor.Experimental neurology · 2013Article
- Cardiac fibroblasts regulate sympathetic nerve sprouting and neurocardiac synapse stability.PloS one · 2013Article
- Remodeling of intrinsic cardiac neurons: effects of β-adrenergic receptor blockade in guinea pig models of chronic heart disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2012Article
- Ciliary neurotrophic factor stimulates tyrosine hydroxylase activity.Journal of neurochemistry · 2012Article
- Dopaminergic modulation of synaptic transmission and neuronal activity patterns in the zebrafish homolog of olfactory cortex.Frontiers in neural circuits · 2012Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Myocardial infarction causes a heterogeneity of noradrenergic transmission that contributes to the development of ventricular arrhythmias and sudden cardiac death. Ischaemia-induced alterations in sympathetic transmission include regional variations in cardiac noradrenaline (NA) and in tyrosine hydroxylase, the rate-limiting enzyme in NA synthesis. Inflammatory cytokines that act through gp130 are elevated in the heart after myocardial infarction. These cytokines decrease expression of tyrosine hydroxylase in sympathetic neurons, and indirect evidence suggests that they contribute to the local depletion of tyrosine hydroxylase in the damaged left ventricle. However, gp130 cytokines are also important for the survival of cardiac myocytes following damage to the heart. To examine the effect of cytokines on tyrosine hydroxylase and NA content in cardiac nerves we used gp130(DBH-Cre/lox) mice, which have a deletion of the gp130 receptor in neurons expressing dopamine beta-hydroxylase. The absence of neuronal gp130 prevented the loss of tyrosine hydroxylase in cardiac sympathetic nerves innervating the left ventricle 1 week after ischaemia-reperfusion compared with wild-type C57BL/6J mice. Surprisingly, restoration of tyrosine hydroxylase in the damaged ventricle did not return neuronal NA content to normal levels. Noradrenaline uptake into cardiac nerves was significantly lower in gp130 knockout mice, contributing to the lack of neuronal NA stores. There were no significant differences in left ventricular peak systolic pressure, dP/dt(max) or dP/dt(min) between the two genotypes after myocardial infarction, but ganglionic blockade revealed differences in autonomic tone between the genotypes. Stimulation of the heart with dobutamine or release of endogenous NA with tyramine generated similar responses in both genotypes. Thus, the removal of gp130 from sympathetic neurons prevents the post-infarct depletion of tyrosine hydroxylase in the left ventricle, but does not alter NA content or cardiac function.
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