First Author | Strain MM | Year | 2024 |
Journal | iScience | Volume | 27 |
Issue | 3 | Pages | 109137 |
PubMed ID | 38420585 | Mgi Jnum | J:348987 |
Mgi Id | MGI:7609611 | Doi | 10.1016/j.isci.2024.109137 |
Citation | Strain MM, et al. (2024) Dorsal motor vagal neurons can elicit bradycardia and reduce anxiety-like behavior. iScience 27(3):109137 |
abstractText | Cardiovagal neurons (CVNs) innervate cardiac ganglia through the vagus nerve to control cardiac function. Although the cardioinhibitory role of CVNs in nucleus ambiguus (CVN(NA)) is well established, the nature and functionality of CVNs in dorsal motor nucleus of the vagus (CVN(DMV)) is less clear. We therefore aimed to characterize CVN(DMV) anatomically, physiologically, and functionally. Optogenetically activating cholinergic DMV neurons resulted in robust bradycardia through peripheral muscarinic (parasympathetic) and nicotinic (ganglionic) acetylcholine receptors, but not beta-1-adrenergic (sympathetic) receptors. Retrograde tracing from the cardiac fat pad labeled CVN(NA) and CVN(DMV) through the vagus nerve. Using whole-cell patch-clamp, CVN(DMV) demonstrated greater hyperexcitability and spontaneous action potential firing ex vivo despite similar resting membrane potentials, compared to CVN(NA). Chemogenetically activating DMV also caused significant bradycardia with a correlated reduction in anxiety-like behavior. Thus, DMV contains uniquely hyperexcitable CVNs and is capable of cardioinhibition and robust anxiolysis. |