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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.<\/jats:p>","DOI":"10.1172\/jci.insight.155747","type":"journal-article","created":{"date-parts":[[2022,1,11]],"date-time":"2022-01-11T13:15:09Z","timestamp":1641906909000},"source":"Crossref","is-referenced-by-count":34,"title":["Myocardial infarction reduces cardiac nociceptive neurotransmission through the vagal ganglia"],"prefix":"10.1172","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3820-1353","authenticated-orcid":true,"given":"Siamak","family":"Salavatian","sequence":"first","affiliation":[{"name":"UCLA Cardiac Arrhythmia Center and"},{"name":"UCLA Neurocardiology Research Program of Excellence, Los Angeles, California, 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