ArticleJCI insight2022
Myocardial infarction reduces cardiac nociceptive neurotransmission through the vagal ganglia.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Spinal nociceptive denervation impedes subsequent chronic autonomic remodeling after myocardial infarction in male swine.Nature communications · 2026Article
- Vagal GABAergic signaling in autonomic control of cardiometabolic function.American journal of physiology. Cell physiology · 2026Review
- The Heart-Brain Axis in the Context of Cardiovascular Disease.Physiology (Bethesda, Md.) · 2026Review
- The brain-heart axis: effects of cardiovascular disease on the CNS and opportunities for central neuromodulation.Nature reviews. Neuroscience · 2026Review
- Selected Large-Animal Models of Ventricular Arrhythmias.Biology · 2026Review
- Analysis of the predictive value of heart rate variability analysis combined with SOFA and APACHE II scores for the 28-day mortality risk of patients in the emergency intensive care unit.Frontiers in medicine · 2026Article
- The vagus nerve as a neurovisceral interface: a comprehensive review.Frontiers in neuroscience · 2026Review
- NF-Frontiers in cardiovascular medicine · 2026Article
- Tyrosine Hydroxylase-Expressing Neurons in the Vagal Ganglia: Characterization and Implications.Biomedicines · 2025Article
- Computational modelling of cardiac control following myocardial infarction using an in silico patient cohort.The Journal of physiology · 2025Article
- Neurocardiology: translational advancements and potential.The Journal of physiology · 2025Review
- Cardiac Sympathetic Innervation and Ventricular Arrhythmias in Structural Heart Disease: Current Peripheral Neuromodulation Therapies and Emerging Therapeutic Targets.Arrhythmia & electrophysiology review · 2025Review
- Improving Sensitivity and Longevity of In Vivo Glutamate Sensors with Electrodeposited NanoPt.ACS applied materials & interfaces · 2024Article
- Antiarrhythmic Mechanisms of Epidural Blockade After Myocardial Infarction.Circulation research · 2024Article
- Myocardial infarction causes sex-dependent dysfunction in vagal sensory glutamatergic neurotransmission that is mitigated by 17β-estradiol.JCI insight · 2024Article
- Mechanism of Ventricular Tachycardia Occurring in Chronic Myocardial Infarction Scar.Circulation research · 2024Review
- Autonomic control of ventricular function in health and disease: current state of the art.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Review
- Cardiac vagal afferent neurotransmission in health and disease: review and knowledge gaps.Frontiers in neuroscience · 2023Review
- Spinal neuromodulation mitigates myocardial ischemia-induced sympathoexcitation by suppressing the intermediolateral nucleus hyperactivity and spinal neural synchrony.Frontiers in neuroscience · 2023Article
- Convergent cardiorespiratory neurons represent a significant portion of cardiac and respiratory neurons in the vagal ganglia.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Myocardial infarction causes pathological changes in the autonomic nervous system, which exacerbate heart failure and predispose to fatal ventricular arrhythmias and sudden death. These changes are characterized by sympathetic activation and parasympathetic dysfunction (reduced vagal tone). Reasons for the central vagal withdrawal and, specifically, whether myocardial infarction causes changes in cardiac vagal afferent neurotransmission that then affect efferent tone, remain unknown. The objective of this study was to evaluate whether myocardial infarction causes changes in vagal neuronal afferent signaling. Using in vivo neural recordings from the inferior vagal (nodose) ganglia and immunohistochemical analyses, structural and functional alterations in vagal sensory neurons were characterized in a chronic porcine infarct model and compared with normal animals. Myocardial infarction caused an increase in the number of nociceptive neurons but a paradoxical decrease in functional nociceptive signaling. No changes in mechanosensitive neurons were observed. Notably, nociceptive neurons demonstrated an increase in GABAergic expression. Given that nociceptive signaling through the vagal ganglia increases efferent vagal tone, the results of this study suggest that a decrease in functional nociception, possibly due to an increase in expression of inhibitory neurotransmitters, may contribute to vagal withdrawal after myocardial infarction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.