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Norepinephrine increases glycinergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus
Author(s) -
Philbin Kerry Elizabeth,
Bateman Ryan,
Reynolds Carie,
Mendelowitz David
Publication year - 2011
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.25.1_supplement.1077.5
Subject(s) - nucleus ambiguus , neurotransmission , norepinephrine , baroreflex , heart rate , medicine , endocrinology , catecholaminergic cell groups , neuroscience , adrenergic receptor , brainstem , catecholaminergic , blood pressure , receptor , catecholamine , biology , medulla oblongata , dopamine , central nervous system
Exaggeration of the noradrenergic system within the brain is a potential source of autonomic imbalance in which sympathetic activity dominates parasympathetic control. Such dysregulation may play a role in the observed increase in heart rate and blood pressure seen in post‐traumatic stress disorder (PTSD). While current research focuses on the enhanced sympathoadrenal activity, little is known about the potentially equally important vagal withdrawal in PTSD. Parasympathetic innervation to the heart originates in premotor cardioinhibitory vagal neurons (CVNs) located in the nucleus ambiguus and the activity of these CVNs largely determine resting heart rate. This study examines the ability of the catecholaminergic neurotransmitter, norepinephrine (NE), to alter glycinergic synaptic inputs to CVNs via α 1 adrenergic receptors. Bath application of either NE or phenylephrine, an α 1 agonist, significantly increased inhibitory glycinergic inputs to CVNs. These data indicate that NE activates α 1 receptors to increase glycinergic neurotransmission to CVNs, resulting in a likely withdrawal of parasympathetic activity to the heart and subsequent increase in heart rate. These results provide a cellular mechanism by which increased NE activity in the brainstem can lead to the increases in heart rate and blood pressure that occur with PTSD and other conditions of exaggerated noradrenergic activity. Supported by NIH grants HL 49965, 59895, 72006 to DM.