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Transcriptional Profiling of Laser Captured Neurons in the Dorsal Motor Nucleus of the vagus in Response to Ischemic Heart Failure
Author(s) -
Gorky Jon,
Vadigepalli Rajanikanth,
Schwaber James
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.580.11
Subject(s) - dorsal motor nucleus , heart failure , interneuron , neuroscience , phenotype , vagus nerve , receptor , biology , myocardial infarction , medicine , inhibitory postsynaptic potential , gene , genetics , stimulation
The dorsal motor nucleus of the vagus (DMV) has been shown to exert a protective effect against damage from myocardial infarction (MI) that may be crucial in preventing subsequent heart failure. A time series of transcriptional changes in 1000 laser captured neurons were studied in a rat model of MI. The results show a significant response after 1 week involving Npff and GABA receptor gene expression changes in neurons. After 3 weeks, there were changes in somatostatin gene expression not seen at 1 week, suggesting increased inhibitory interneuron activity. The was an overall constraining of the diversity of transnational phenotype in response to ischemia both at one week and three weeks. Several of these responses showed left/right asymmetry, with a bias toward changes on the right. Gene regulatory network topology was also significantly altered, showing the potential for the orexin‐2 receptor to be a novel regulatory hub. This represents the first time single neurons in the DMV have been assayed in response to ischemic heart failure and the results suggest new ways in which the DMV modulates protective effects at the heart. Support or Funding Information Funding Sources: T32 AA007463‐28; U01 HL133360; RO1 HL111621‐01A1; OT2 ‐ SPARCThe DMV mediates a cardioprotective effect via multiple outputs not only through direct connections with the heart, but also via connections to secretory endocrine cells in gut.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .