{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T13:47:20Z","timestamp":1791380840233,"version":"4.3.3"},"reference-count":68,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2016,4,28]],"date-time":"2016-04-28T00:00:00Z","timestamp":1461801600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2016,7,15]]},"abstract":"<jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>The strength, functional significance and origins of parasympathetic innervation of the left ventricle remain controversial.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>This study tested the hypothesis that parasympathetic control of left ventricular contractility is provided by vagal preganglionic neurones of the dorsal motor nucleus (DVMN).<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Under \u03b2\u2010adrenoceptor blockade combined with spinal cord (C1) transection (to remove sympathetic influences), systemic administration of atropine increased left ventricular contractility in rats anaesthetized with urethane, confirming the existence of a tonic inhibitory muscarinic influence on cardiac inotropy.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Increased left ventricular contractility in anaesthetized rats was observed when DVMN neurones were silenced.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Functional neuroanatomical mapping revealed that vagal preganglionic neurones that have an impact on left ventricular contractility are located in the caudal region of the left DVMN.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>These neurones provide functionally significant parasympathetic control of left ventricular inotropy.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      The strength, functional significance and origins of direct parasympathetic innervation of the left ventricle (LV) remain controversial. In the present study we used an anaesthetized rat model to first confirm the presence of tonic inhibitory vagal influence on LV inotropy. Using genetic neuronal targeting and functional neuroanatomical mapping we tested the hypothesis that parasympathetic control of LV contractility is provided by vagal preganglionic neurones located in the dorsal motor nucleus (DVMN). It was found that under systemic \u03b2\u2010adrenoceptor blockade (atenolol) combined with spinal cord (C1) transection (to remove sympathetic influences), intravenous administration of atropine increases LV contractility in rats anaesthetized with urethane, but not in animals anaesthetized with pentobarbital. Increased LV contractility in rats anaesthetized with urethane was also observed when DVMN neurones targeted bilaterally to express an inhibitory\n                      <jats:italic>Drosophila<\/jats:italic>\n                      allatostatin receptor were silenced by application of an insect peptide allatostatin. Microinjections of glutamate and muscimol to activate or inhibit neuronal cell bodies in distinct locations along the rostro\u2010caudal extent of the left and right DVMN revealed that vagal preganglionic neurones, which have an impact on LV contractility, are located in the caudal region of the left DVMN. Changes in LV contractility were only observed when this subpopulation of DVMN neurones was activated or inhibited. These data confirm the existence of a tonic inhibitory muscarinic influence on LV contractility. Activity of a subpopulation of DVMN neurones provides functionally significant parasympathetic control of LV contractile function.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp270984","type":"journal-article","created":{"date-parts":[[2016,3,5]],"date-time":"2016-03-05T12:12:59Z","timestamp":1457179979000},"page":"4017-4030","source":"Crossref","is-referenced-by-count":58,"title":["Origins of the vagal drive controlling left ventricular contractility"],"prefix":"10.1113","volume":"594","author":[{"given":"Asif","family":"Machhada","sequence":"first","affiliation":[{"name":"Centre for Cardiovascular and Metabolic Neuroscience, Neuroscience, Physiology and Pharmacology University College London  London WC1E 6BT UK"},{"name":"UCL Centre for Advanced Biomedical Imaging, Division of Medicine University College London  London WC1E 6DD UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nephtali","family":"Marina","sequence":"additional","affiliation":[{"name":"Centre for Cardiovascular and Metabolic Neuroscience, Neuroscience, Physiology and Pharmacology University College London  London WC1E 6BT UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alla","family":"Korsak","sequence":"additional","affiliation":[{"name":"Centre for Cardiovascular and Metabolic Neuroscience, Neuroscience, Physiology and Pharmacology University College London  London WC1E 6BT UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel J.","family":"Stuckey","sequence":"additional","affiliation":[{"name":"UCL Centre for Advanced Biomedical Imaging, Division of Medicine University College London  London WC1E 6DD UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark F.","family":"Lythgoe","sequence":"additional","affiliation":[{"name":"UCL Centre for Advanced Biomedical Imaging, Division of Medicine University College London  London WC1E 6DD UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander V.","family":"Gourine","sequence":"additional","affiliation":[{"name":"Centre for Cardiovascular and Metabolic Neuroscience, Neuroscience, Physiology and Pharmacology University College London  London WC1E 6BT UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,4,28]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.2001.00812.x"},{"key":"e_1_2_6_3_1","first-page":"H854","article-title":"In vivo detection of endogenous acetylcholine release in cat ventricles","volume":"266","author":"Akiyama T","year":"1994","journal-title":"Am J Physiol"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.1981.sp002541"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1002\/1096-9861(20000904)424:4<588::AID-CNE3>3.0.CO;2-7"},{"key":"e_1_2_6_6_1","first-page":"R57","article-title":"Distribution of vagal cardioinhibitory neurons in the medulla of the cat","volume":"238","author":"Ciriello J","year":"1980","journal-title":"Am J Physiol"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(82)90086-8"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1161\/hh1501.094266"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00135.2002"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2013.257758"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1469-7580.1999.19530359.x"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.144.3623.1223"},{"key":"e_1_2_6_13_1","doi-asserted-by":"crossref","first-page":"564","DOI":"10.1152\/ajplegacy.1965.209.3.564","article-title":"Carotid chemoreceptor stimulation and ventricular performance","volume":"209","author":"Degeest H","year":"1965","journal-title":"Am J Physiol"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.17.4.349"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.17.3.222"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00130.2002"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1177\/002215540104901004"},{"key":"e_1_2_6_18_1","first-page":"1372","article-title":"Effect of vagal stimulation and acetylcholine on the ventricle. 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